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Objective To investigate changes and clinical significance of serum microRNA-155 (miR-155) and microRNA-205-5p (miR-205-5p) levels in patients with hepatitis C virus (HCV) infection. Methods A total of 141 patients with HCV infection were collected and divided into the HCV-1b group (92 cases) and the non HCV-1b group (49 cases) according to their genotype, and another 141 healthy volunteers who underwent physical examinations in our hospital during the same period were collected as the control group. The general information, biochemical indicators and serum levels of miR-155 and miR-205-5p were compared between the three groups. According to the grading of hepatitis activity, HCV infected patients were classified into the G0, G1, G2, G3 and G4 groups, and serum levels of miR-155 and miR-205-5p were compared between the five groups. Receiver operating characteristics (ROC) curve was used to analyze clinical values of serum miR-155 and miR-205-5p in diagnosing hepatitis activity of G1-G4 in patients with HCV infection. Results The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and total bilirubin (TBIL) were obviously higher in the HCV-1b group and the non HCV-1b group than those in the control group, while the level of ALB was obviously lower than that in the control group (P＜0.05). The serum level of miR-155 was increased in turn in the control group, the nonHCV-1b group and the HCV-1b group, and the serum level of miR-205-5p was decreased in turn (P＜0.05). The serum level of miR-155 increased in turn with the increased grading of hepatitis activity, while the serum miR-205-5p level decreased in turn (P＜0.05). The area under curve (AUC) values of serum miR-155, miR-205-5p and their combination in diagnosing hepatitis activity of G1-G4 in HCV infected patients were 0.855, 0.793 and 0.913, respectively, and the combination of the two is superior to each individual diagnosis (P＜0.05). Conclusion The serum miR-155 level increases and miR-205-5p level decreases in HCV infected patients. The combination of the two has high efficacy in diagnosing hepatitis activity of G1-G4 in HCV infected patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the relationship between the expression of microRNA-155 (mi R-155) and microRNA-202 (mi R-202) and the expression of proliferation and invasion genes, clinicopathological parameters and prognosis in endometrial carcinoma (EC) tissue. Methods: 135 EC patients who were underwent surgical treatment in our hospital from October 2015 to October 2018 were selected as observation group, and 135 patients with uterine fibroids who were underwent total hysterectomy during the same period were selected as control group, the expression of mi R-155, mi R-202 and proliferation genes (Cdk4, Cdk6, Efemp2, DJ-1, RRM2) and invasion genes (Dkk1, Ezh2, HMGB1) in two groups were detected and compared by real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), the relationship between the expression of mi R-155 and mi R-202 in EC tissues and the clinicopathological parameters of patients were analyzed. The 5 years cumulative survival rate of high expression and low expression of mi R-155 and mi R-202 were analyzed by Kaplan-Meier survival curve. Results: The relative expression levels of mi R-155, Ezh2, HMGB1, Cdk4,Cdk6, DJ-1 and RRM2 in observation group were higher than those in control group, and the relative expression levels of mi R-202, Dkk1and Efemp2 were lower than those in control group (P＜0.05). The relative expression of mi R-155 was positively correlated with Cdk4,Cdk6, DJ-1, RRM2, Ezh2 and HMGB1, and negatively correlated with Efemp2 and Dkk1 (P＜0.05). The relative expression of mi R-202was positively correlated with Efemp2 and Dkk1, and negatively correlated with Cdk4,Cdk6, DJ-1, RRM2, Ezh2 and HMGB1 (P＜0.05). The higher the FIGO stage of EC patients, the lower the degree of differentiation, the deeper the myometrial invasion and the higher the relative expression of mi R-155 in patients with lymph node metastasis, the lower the relative expression of mi R-202 (P＜0.05). The 5years overall survival rate in high mi R-155 group was 68.66%, which was lower than that 87.50% in low mi R-155 group (P＜0.05). The 5years survival rate in high mi R-202 group was 91.80%, which was higher than that 65.71% in low mi R-202 group (P＜0.05). Conclusion: The expression of mi R-155 increase and the expression of mi R-202 decrease in EC tissues, which are significantly correlate with the expression of proliferation and invasion genes, FIGO stage, differentiation degree, depth of myometrial invasion and lymph node metastasis, the higher the expression of mi R-155, the lower the expression of mi R-202, and the worse the prognosis of patients. [ABSTRACT FROM AUTHOR]

BACKGROUND: Abnormal activation of osteoclasts plays an important role in the bone destruction due to spinal tuberculosis. During the pathogenesis of osteoporosis, miR-155 knockdown activates adenosine phosphate-dependent protein kinase (AMPK) by increasing the expression of leptin receptors, thereby inhibiting osteoclast differentiation and bone resorption. However, the role of miR-155/leptin receptor(LEPR)/AMPK axis in the bone destruction due to spinal tuberculosis remains unclear. OBJECTIVE: To investigate the role and mechanism of miR-155/LEPR/AMPK axis in tuberculin-induced osteoclast formation. METHODS: RAW264.7 cells were cultured and treated with different concentrations of purified protein derivative (PPD) (1.0, 2.5, 5.0, 10.0 IU/mL) and transfected with negative control (NC) sequence or miR-155 inhibitor, NC siRNA sequence or LEPR siRNA sequence. Tartrate resistant acid phosphatase staining was used to detect the number of osteoclasts. Fluorescence quantitative PCR was used to detect the expression of miR-155. Western blot was used to detect the expression of LEPR and p-AMPK. Double luciferase reporter gene was used to verify miR-155 targeting LEPR. RESULTS AND CONCLUSION: Compared with the control group, the number of osteoclasts and the expression level of miR-155 significantly increased, while the expression level of LEPR and p-AMPK significantly decreased in 2.5, 5.0, and 10.0 IU/mL PPD groups (P < 0.05). Compared with NC+5.0 IU/mL PPD group, the number of osteoclasts and the expression level of miR-155 significantly decreased, while the expression level of LEPR and p-AMPK significantly increased in the miR-155 inhibitor+5.0 IU/mL PPD group (P < 0.05). Compared with the NC group, the fluorescence activity of LEPR wild-type double luciferase reporter gene was increased in the miR-155 inhibitor group, and decreased in the miR-155 mimic group (P < 0.05). Compared with si-NC+miR-155 inhibitor+5.0 IU/ mL PPD group, the expression level of miR-155 had no significant change, the number of osteoclasts significantly increased, and the expression levels of LEPR and p-AMPL significantly decreased in si-LEPR+miR-155 inhibitor+5.0 IU/mL PPD group (P < 0.05). To conclude, tuberculin can induce osteoclast formation by increasing miR-155 expression and inhibiting downstream LEPR expression and AMPK activation. [ABSTRACT FROM AUTHOR]

Objective This research aimed to investigate the expression and mechanism of miR-155 and suppressor of cytokine signaling 1 (SOCS1) in rheumatoid arthritis (RA). Methods RT-PCR and flow cytometry were applied to detect the expression differences of miR-155, Th17, and Treg cells in peripheral blood of RA patients (RA group) and control group (HC group). Bioinformatics analysis and dual-luciferase reporter assay were conducted to investigate the regulatory relationship between miR-155 and SOCS1. CD4+T cells were isolated from peripheral blood of RA patients and transfected with miR-155 inhibitor, si-SOCS1, and their respective negative control sequences, and divided into four groups: miR-NC group, miR-155 inhibitor group, miR-155 inhibitor+ si-NC group, and miR-155 inhibitor+si-SOCS1 group. The cells were treated with Th17-inducing differentiation medium, and flow cytometry was used to determine the ratio of Th17 cells in each group of CD4+T cells. Western blot was used to determine the ratio of p-STAT3/STAT3 in the cells. Results Compared to the HC group, RA patients showed increased expression of miR-155 and Th17 ratio (P < 0.01), and decreased Treg cell ratio (P < 0.01). MiR-155 could target and inhibit the expression of SOCS1. Compared to the miR-NC group, the miR-155 inhibitor group, miR-155 inhibitor+si-NC group, and miR-155 inhibitor+si-SOCS1 group showed decreased Th17 ratio and p-STAT3/STAT3 ratio (P < 0.01). Compared to the miR-155 inhibitor group, the miR-155 inhibitor+ si-SOCS1 group exhibited increased Th17 ratio and p-STAT3/STAT3 ratio in CD4+T cells (P < 0.05). Conclusio through the SOCS1/STAT3 pathway, contributing to the imbalance of Th17/Treg cells in peripheral blood of RA patients. [ABSTRACT FROM AUTHOR]

Objective To investigate the efficacy of lomefloxacin combined with triamcinolone olone in the treatment of acute otitis media (AOM) in children and the effects on serum miR-203a and miR-155. Meth ods According to different treatment methods, 134 children with AOM in our hospital from June 2021 to June 2023 were divided into the control group and the combination group, with 67 cases in each group. The control group was treated with triamcinolone and the combination group was treated with lomefloxacin anc triamcinolone. The clinical efficacy, recovery time, inflammatory factors [interleukin-8 (IL-8), procalcitonin (PCT), tumor necrosis factor(TNF-a)], serum levels of miR-203a and miR-155, pathogenic bacteria clearanc and adverse reactions were compared between the two groups. Results The total effective rate of combinee group [92.54% * (62/67)] was higher than that of control group [80.6% * (54/67)] the difference was statisti cally significant (P < 0.05) Compared with the control group, the hearing recovery time, tympanic congestion fading time earache fading time and fever fading time of the combined group were shorter after treatment, the difference were statistically significant (P < 0.05) Compared with before treatment. IL-8, TNF-a, PCT, miR 155 and miR-203a in the combination group were significantly decreased after treatment P < 0.05 ) The path ogenic bacteria clearance rate of the combined group [91.04% (61/67)] was higher than that of the contro group [77.61%(52/67)], the difference was statistically significant (P < 0.05), and there was no significan difference in the total incidence of adverse reactions between the two groups (P > 0.05) . Conclusion Lome floxacin combined with triamcinolone in the treatment of AOM is effective, can reduce inflammation by down. regulating the levels of miR-203a and miR-155, can also improve the clearance rate of pathogenic bacteria, pro mote disease recovery, and has high safety. [ABSTRACT FROM AUTHOR]

Objective: To establish a mouse model of breast cancer lung metastasis with miR-155 knockout (miR155-/-) mice, and to compare the difference of peripheral blood immune cell typing between miR155-/- mice and C57BL/6J wide-type (WT) mice. Methods: Bioinformatics analysis was used to explore the expression level of miR-155 in breast cancer tissues and peripheral serum, and its relationship with prognosis. Mouse model of lung metastasis of breast cancer was established by tail vein injection; peripheral blood was collected for flow cytometry, and the immune cell typing was analyzed; the lung tissues were collected for immunohisto-chemical detection to observe the tumor metastasis. Results: Percentage of T lymphocytes and monocytes in peripheral blood of miR155-/- mice was significantly decreased compared with WT mice (P<0.05), percentage of myeloid inhibitory cells (MDSCs) was increased significantly (P<0.05), in which the proportion of monocyte subsets (M-MDSC) was significantly decreased (P<0.05), while the proportion of granulocyte subsets (G-MDSC) was significantly increased (P<0.05). In lung metastasis model of breast cancer, percentage of T lymphocytes in peripheral blood of miR155-/- mice was significantly higher compared with WT mice, while percentage of NK cells was decreased significantly (P<0.05), percentage of neutrophil was significantly decreased (P<0.001), proportion of Th cells in T lymphocytes was significantly decreased (P<0.05), proportion of M-MDSCs was significantly decreased (P< 0.01), while proportion of G-MDSCs was significantly increased (P<0.01). Conclusion: Deletion of miR-155 gene leads to significant differences in peripheral immune cell typing, making mice more susceptible to lung metastasis of breast cancer. [ABSTRACT FROM AUTHOR]

Allergic rhinitis (AR) is a type I allergic reaction, which mediated by immunoglobulin E immediately when an individual with a special constitution is exposed to a same allergen for second time, whose pathogenesis has not been clarified yet, and closely related to genes, immune cells and cytokines. Pathogenesis of AR become more deeper and more accurate due to rapid develop-ment of molecular biology and second-generation gene sequencing technology. Current studies have found that miR-155 and transcription factor GATA3 have important regulatory effects on occurrence and development of AR, then affect dominant differentiation of CD4+T lymphocytes and proliferation of ILC2. This article discusses and reviews pathogenesis of AR, which mainly focuses on miR-155/GATA3 pathway and effects of related upstream genes and downstream regulatory substances. [ABSTRACT FROM AUTHOR]

Objective: Exploring the effects of miR-155 regulation of SMAD2 expression in podocyte injury as well as macrophage inflammatory response in mouse lupus nephritis. Methods: The experimental mice were randomly divided into blank, model, AAV9-miR-NC, AAV9-miR-155, AAV9-miR-anti, and AAV9-miR-anti-NC groups, with 8 mice in each group, of which the blank group was C57BL/6 mice, and the rest of the groups were MRL/lpr mice, and the groups were treated and sampled accordingly. The presence or absence of a binding site for miR-155 and SMAD2 was predicted by target genes, an online target gene prediction website. Dual luciferase reporter gene analysis system to validate the targeting relationship between miR-155 and SMAD2. Determination of 24 h urinary protein content in each group of mice by Caumas Brilliant Blue method. Hematoxylin-Eosin staining was used to observe the kidney tissues of mice ; qRT-PCR to detect the expression level of miR-155 in kidney tissues of each group. Western blot was used to detect nephrin, P-cadherin and SMAD2 protein expression in renal tissues. Immunofluorescence assay to detect the expression of inflammatory factors (IL-6, TNF-α) in mice. Results: Compared with the blank group, mice in the model group had elevated urinary protein, severe renal pathological damage, and decreased expression levels of nephrin, P-cadherin, and SMAD2 while increased expression levels of IL-6 and TNF-α in renal tissues (P<0.05). Compared with the model group and AAV9-miR-NC group, mice in the model group of AAV9- miR-155 group showed elevated urinary protein, obvious renal pathological damage, and obvious elevation of miR-155 in renal tissues, whereas the expression levels of nephrin, P-cadherin, and SMAD2 were decreased (P<0.05) whereas the fluorescence intensity of IL-6 and TNF-α was enhanced significantly; Compared with the model and AAV9-miR-anti-NC groups, mice in the AAV9-miR-anti group showed decreased urinary protein, improved renal pathological injury, decreased miR-155 expression, and increased expression levels of nephrin, P-cadherin, and SMAD2 compared to the model group (P<0.05) whereas the fluorescence intensities of IL-6 and TNF-α decreased; In the model group, AAV9-miR-NC group, and AAV9-miR-anti-NC group mice, the differences in the above indexes were not statistically significant (P>0.05). Dual luciferase reporter gene assay showed that miR-155 inhibited the fluorescence activity of wild-type SMAD2 cells and targeted the regulation of SMAD2 expression. Conclusion: High expression of miR-155 exacerbated podocyte injury and inflammatory response in lupus nephritis in mice by regulating SMAD2, whereas inhibition of miR-155 expression attenuated podocyte injury and inflammatory response in mice. [ABSTRACT FROM AUTHOR]

Objective To explore the prognostic value of serum levels of miR-155 and Smad5 in hemodialysis (HD) patients with acute renal failure (ARF). Methods From August 2018 to July 2019, 120 ARF patients on HD were selected as study group while another 116 healthy subjects as control group; the serum expressions of miR-155 and Smad5 mRNA were detected by quantitative reverse transcriptase-mediated polymerase chain reaction (qRT-PCR). Pearson’s method was utilized for examining the correlation between serum expression levels of miR-155 and Smad5 mRNA and the levels of creatinine and blood urea nitrogen (BUN); Kaplan-Meier method was employed for examining the survival of HD patients with ARF; COX regression for analyzing the prognostic factors; receiver operating characteristic curve (ROC) curve for assessing the predictive value of serum miR-155 and Smad5 mRNA levels. Results The levels of serum miR-155, creatinine and BUN were obviously higher in study group than those in control group (P

Background and objective There is a high morbidity, mortality, and poor clinical prognosis of lung squamous cell carcinoma (LUSC). However, there is currently no effective targeted treatment plan for LUSC. As a long non-coding RNA (lncRNA), lncRNA miR143HG has been proven to play an important role in the occurrence and development of various tumors. However, the biological role played by lncRNA miR143HG in LUSC cells is still unclear. Therefore, this study aimed to investigate the mechanism of lncRNA miR143HG on regulating the biological behavior of LUSC H520 cells. Methods Pan-cancer analysis and differential expression analysis of lncRNA miR143HG were performed based on The Cancer Genome Atlas (TCGA) database. The predictive effect of lncRNA miR143HG on the diagnosis and prognosis of LUSC was evaluated by adopting the receiver operating characteristic (ROC) curve and timeROC curve. The enrichment degree of each pathway to lncRNA miR143HG was determined. The expression of lncRNA miR143HG and miR-155 in BEAS-2B cells and H520 cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). H520 cells were randomly divided into blank control group (without any treatment), negative control group (transfected with lncRNA-NC), lncRNA miR143HG group (transfected with lncRNA miR143HG), and lncRNA miR143HG+miR-155 group (co-transfected with lncRNA miR143HG and miR-155). The approaches of CCK-8, wound healing test, Transwell assay, flow cytometry, qRT-PCR, and Western blot were respectively employed to detect the cell proliferation ability, cell migration ability, cell invasion ability, cell apoptosis rate, and expression level of related genes and proteins of the Wnt/β-Catenin pathway. Results The results of pan-cancer analysis and differential analysis collectively showed that except for renal clear cell carcinoma, the expression of lncRNA miR143HG in other cancer tissues was higher than that in healthy tissues, and the differences were significant in LUSC. The evaluation results of the ROC curve and timeROC curve suggested that lncRNA miR143HG was of great significance in the prediction of diagnosis and prognosis of LUSC. The pathways enriched in high expression of lncRNA miR143HG mainly included focal adhesion, vascular smooth muscle contraction, calcium signaling pathways, and so on; the pathways enriched in the low expression of lncRNA miR143HG embraced oxidative phosphorylation, cell cycle, basic transcription factors, etc. The qRT-PCR results showed that lncRNA miR143HG was low expressed but miR-155 was highly expressed in H520 cells when compared to BEAS-2B cells (P

Objective To investigate the identification of octreotide (OCT) modified chitosan (CS) miR-155 molecular beacon nanoparticles (CS-miR-155-MB-OCT) and imaging of lung cancer cells for the early screening of lung cancer. Methods A nude mouse model of lung transplantation tumor was established by injecting A549 lung cancer cells into tail veins to establish lung xenograft models. Cre adenovirus was injected through nasal cavity, and mice were killed at 4, 6, 8 and 12 weeks after adenovirus injection to establish lung cancer models of atypical hyperplasia, adenoma, carcinoma in situ and adenocarcinoma of lung in LSL K-ras G12D transgenic mice at different pathological stages. Lung tissue samples were taken and observed by HE staining. Immunohistochemistry were used to detect the expression of somatostatin receptor 2 (SSTR2). Real-time fluorescence quantitative PCR was used to detect miR-155 expression levels in lung xenograft models and transgenic mice at different stages of lung cancer. Then CS-miR-155-MB and CS-miR-155-MB-OCT were injected via tail vein in lung xenograft models. CS-miR-155-MB-OCT was injected via tail vein in transgenic mice models. The fluorescence signals of lung in nude mice and transgenic mice at different disease stages were imaged by living imaging system. Frozen slices of lung tissue were made. The source of fluorescence signal was detected by laser confocal scanning microscope (CLSM). Results HE staining showed that lung transplantation tumor models and lung cancer models of atypical hyperplasia, adenoma, carcinoma in situ and lung adenocarcinoma at different pathological stages were successfully constructed. Immunohistochemical analysis showed somatostatin receptor 2 (SSTR2) was expressed in transplanted lung tumor and tissue at different pathological stages. In transgenic mouse models，the expression of miR-155 was gradually increased as the disease progressed (P＜0.05). In lung xenograft models, the fluorescence signals were significantly higher in the CS-miR-155-MB-OCT group than those of the CS-miR-155-MB group (P＜0.05). In transgenic mouse models, the fluorescence signals gradually increased with the gradual progression of lesions (P＜0.05). After re-imaging the lung tissue, it was found that the fluorescence signal came from lung, and CLSM showed that the fluorescence signal came from cancer cells and some normal alveolar epithelial cells. Conclusion CS-miR-155-MB-OCT can dynamically reflect the occurrence and development of lung cancer according to changes of different fluorescence intensity, thus providing a new technology for the early diagnosis of lung cancer. [ABSTRACT FROM AUTHOR]

Preeclampsia is a pregnancy-specific complication, and hypertension is the main feature of preeclampsia.At present, preeclampsia is still an important cause of maternal and fetal morbidity and mortality, and its pathogenesis is still unclear.The immune intolerance of pregant women to allogeneic embryos is one of the important mechanisms of preeclampsia.miR-155 has important value in the regulation of immune function and can accurately regulate the expression of interleukin-17A.Suppressor of cytokine signaling 1（SOCS1） has been reported to be the only direct target of miR-155 in CD4+T cells and has the biological function of regulating T cell differentiation.This paper preliminarily expounded that miR-155 in placental-derived exosomes affects the differentiation of Treg cells and Th17 cells and the production of IL-17 by inhibiting SOCS1 and regulating JAK/STAT pathway, which provided theoretical guidance for the prevention, diagnosis and treatment of preeclampsia. [ABSTRACT FROM AUTHOR]

Objective: To investigate the correlation between serum micro ribonucleic acid (mi R) -326 and mi R-155 with thyroid-associated antibodies and T helper cell 17 (Th17) /regulatory T cell (Treg) cytokine imbalance in patients with hashimoto thyroiditis (HT) . Method: 82 HT patients who were admitted to Tangdu Hospital of Air Force Military Medical University from January2021 to October 2022 were selected as study group, and 80 healthy individuals who underwent physical examinations as control group during the same period, the levels of serum mi R-326, mi R-155, thyroid function parameters [thyroid stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4) ], thyroid-associated antibodies [thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb) ], Th17, Treg and their cytokine levels were compared between two group, the correlation between serum mi R-326, mi R-155 and thyroid-associated antibodies and Th17/Treg cytokine imbalance in HT patients were analyzed. Results: TSH, TPOAb and TGAb in study group were significantly higher than those in control group, FT3and FT4were significantly lower than those in control group (P＜0.05) . The expression levels of serum mi R-326 and mi R-155 in study group were significantly higher than those in control group (P＜0.05) .Th17, Th17/Treg, interleukin-17 (IL-17) and interferon-γ (IFN-γ) in study group were significantly higher than those in control group, the levels of Treg and interleukin-10 (IL-10) were significantly lower than those in control group (P＜0.05) . Pearson correlation analysis showed that, the serum mi R-326 and mi R-155 in HT patients were positively correlated with TSH, TPOAb, TGAb, Th17, Th17/Treg,IL-17 and IFN-γ respectively, and were negatively correlated with FT3, FT4, Treg and IL-10 (P＜0.05) . Conclusion: The levels of serum mi R-326 and mi R-155 in HT patients are abnormally increase, which level is relate to TPOAb, TGAb autoantibodies and Th17/Treg imbalance, serum mi R-326 and mi R-155 may affect Th17/Treg immune balance, and promote the occurrence and development of HT. [ABSTRACT FROM AUTHOR]

CEBPB具有调节黄体生成促进排卵的作用，对动物繁殖性能极为重要，试验旨在通过构建CEBPB的3'端非翻译区（3'UTR）双荧光素酶报告基因载体，验证MicroRNA-155（miR-155）调控CEBPB的分子机制。应用在线生物信息学软件预测miR-155与CEBPB基因3'UTR的靶向结合区，PCR扩增获取民猪组织基因组的CEBPB的3'UTR，将其插入psi-Check-2载体，构建野生型（wt-3'UTR）和突变型重组表达载体（mut-3'UTR），鉴定正确后，分别与miR-155模拟物（mimics）/抑制物（inhibitor）/阴性对照物（NC）共转染到PK15细胞，检测荧光素酶活性及CEBPB表达情况。结果表明：成功构建了CEBPB的3'UTR野生型和突变型表达载体，双荧光素酶报告基因检测显示wt-3'UTR/miR-155 mimics组的萤火虫荧光素酶活性受到显著抑制（pp>0.05）。实时荧光定量结果显示，miR-155 mimics组CEBPB、BMP1和PPARG表达水平显著低于miR-155 NC组（pCEBPB表达水平高于miR-155 NC组（p<0.05）。综上表明，miR-155可以靶向负调控CEBPB的表达。

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Objective To investigate the expression levels of miR-155 and cGMP-dependent protein kinase 1 (PKG1) in placental tissue of patients with preeclampsia, and the effect of miR-155 on the function of trophoblasts HTR8/SVneo by inhibiting PKG1 under the mediation of nucleus factor kappa B (NF-κB). Methods Twenty placentas were collected from normal pregnant women and pre-eclampsia pregnant women who delivered by cesarean section. In vitro trophoblasts HTR-8/SVneo were cultured and divided into the NC group, the mimics group, the inhibitor group, the siRNA NC group, the PKG1 siRNA group and the siRNA+inhibitor group. Cells were treated with NF- κB inhibitor PDTC and divided into the control group, the PDTC group, the PDTC+NC group and the PDTC+mimics group. Realtime quantitative polymerase chain reaction (qPCR) was performed to detect the expression of miR-155 and PKG1 mRNA in placentas and HTR-8/SVneo cells. Western blot assay was performed to measure the level of PKG1 protein. The cell proliferation, migration and apoptosis were assessed by CCK-8 assay, Transwell assay and flow cytometry. Results The expression of miR-155 was significantly upregulated in placental tissue of the PE group, while the expression of PKG1 decreased significantly (P＜0.05). The vitro experiments showed that compared with the NC group, the expression of PKG1 was significantly reduced in the miR-155 mimics group (P＜0.05). The migration and proliferation ability of trophoblast was significantly weakened, the apoptotic ability was significantly enhanced (P＜ 0.05). The expression of PKG1 was significantly increased in the miR-155 inhibitor group, the migration and proliferation ability of trophoblast was significantly enhanced, and the apoptotic ability was significantly weakened. Compared with the control group, the expression of miR-155 was significantly reduced in the PDTC group, the migration and proliferation ability of trophoblast was significantly enhanced, and the apoptotic ability was significantly weakened (P＜0.05). Conclusion Results indicate that the expression of miR-155 is upregulated in preeclampsia, and can affect proliferation, migration and apoptosis of trophoblast cells by down-regulating PKG1 mediated by NF-κB. [ABSTRACT FROM AUTHOR]

Objective To screen out the target genes of miR-155 associated with immune infiltration in atopic der⁃ matitis (AD), and to verify them by cell experiments. Methods The gene expression profiles of AD (GSE121212 and GSE157194) were obtained from the GEO database, and the differentially expressed genes in AD lesions were screened out. GO functional enrichment analysis and KEGG pathway enrichment analysis were performed, and protein-protein inter⁃ action (PPI) network was constructed. Based on CIBERSORT algorithm, the infiltration of immune cells in AD patients was analyzed. The miRNet website was used to predict the target genes of miR-155, and the target genes related to AD im⁃ mune infiltration were screened. Human immortalized epidermal cells (HaCaT cells) were divided into the control group and TI group. The cells in the TI group were treated with TNF-α and IFN-γ to construct the inflammation models, and the cells in the control group were cultured routinely. The qRT-PCR was used to detect miR-155 in the TI group and control group. The HaCaT cells in the TI group were divided into the TI+miR-155 mimics group and TI+mimics NC group. The HacaT cells in the TI+miR-155 mimics group were transfected with miR-155 overexpression plasmid, and cells in the TI+mimics NC group were transfected with the control plasmid mimics NC. The mRNA levels of CXCL1 and CXCL8 in the TI+miR-155 mimics group and TI+mimics NC group were detected by qRT-PCR. Results A total of 519 differentially expressed genes were identified in AD lesions. GO functional enrichment analysis showed that the differentially expressed genes were mainly involved in biological processes such as immune system process, immune response, response to external stimuli, defense response, and regulation of the immune system. KEGG pathway enrichment analysis showed that, path⁃ ways were mainly enriched in cytokine-cytokine receptor interaction, viral protein-cytokine and cytokine receptor interac⁃ tion, chemokine signaling pathway, IL-17 signaling pathway and other inflammation-related signaling pathways. A PPI network graph consisting of 67 nodes and 146 edges was successfully constructed. Dendritic cells, M2 macrophages and mast cells accounted for the highest proportion in the epidermal immune microenvironment, and the immune infiltra⁃ tion was the most obvious. The target genes of miR-155 were CXCL1 and CXCL8, which were highly correlated with AD immune infiltration. The relative expression of miR-155 in the TI group was higher than that in the control group (P< 0. 05) . The relative expression levels of CXCL1 and CXCL8 mRNA in the TI+miR-155 mimics group were higher than those in the TI+mimics NC group (all P<0. 05) . Conclusions CXCL1 and CXCL8 are the target genes of miR-155 asso⁃ ciated with immune infiltration in AD. High expression of miR-155 increases the expression levels of CXCL1 and CXCL8 genes in HaCaT cells during inflammation. [ABSTRACT FROM AUTHOR]

Objective: To investigate the mechanism of Mir-155 in intestinal tissue injury caused by sepsis. Methods: (1) Clinical experiment: Sepsis patients admitted to the Department of Critical Care Medicine of the First Affiliated Hospital of Xinjiang Medical University from May 2022 to August 2022 and healthy subjects during the same period were selected as the research objects. According to the grade of acute gastrointestinal injury (AGI), sepsis patients were divided into AGI group and non-AGI group. According to the 28-day survival, the patients were divided into survival group and death group. The changes of MiR-155 in peripheral blood of each group were prospectively observed by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). (2) In vivo experiment: Twenty male S/D rats were randomly divided into sham group (Sham group) and cecal ligation and perforation group (CLP group). The expressions of MiR-155 and intestinal tight junction proteins (ZO-1 and claudin-1) were detected by qRT-PCR and Western blot. The expression levels of IL-1β, IL-6 and IL-18 in rat intestinal tissues were determined by ELISA. (3) In vitro experiment: human colorectal adenocarcinoma cells (Caco-2) were cultured and divided into normal control group (complete culture medium for 48 h) and LPS group (complete culture medium for 24 h and then add 10 μg/mL LPS for 24 h). The expression of MiR-155 was detected by qRT-PCR. The changes of cell morphology were observed under an inverted fluorescence microscope. Cell viability was detected by CCK-8. The changes of intestinal tight junction protein (ZO-1) were observed by immunofluorescence. Transwell chamber was used for paracellular permeability test to observe the changes of paracellular permeability between the two groups. Results: (1) Compared with healthy control group, peripheral blood miR-155 in sepsis group was significantly higher than that in healthy control group, with statistical significance (P<0.05). The expression of miR-155 in peripheral blood of AGI group was significantly higher than that of non-AGI group, with statistical significance (P<0.05). The expression of miR-155 in peripheral blood of patients with sepsis death was significantly increased (P<0.05). (2) In vivo animal experiments using the CLP model showed that the expression of miR-155 in the intestinal tissues of rats in the CLP group was significantly higher than that in the sham group. Intestinal compact junction proteins (ZO-1 and claudin-1) in CLP group were decreased compared with those in sham group, and the difference was statistically significant (P<0.05). ELISA results indicated that the levels of IL-1β, IL-6 and IL-18 in the intestinal tissue of CLP rats were significantly higher than those of the sham group (P<0.05), and the level of miR-155 in the intestinal tissue was positively correlated with IL-1β, IL-6 and IL-18(r=0.542, r=0.906, r=868). P<0.05). (3) Compared with the control group, the cell morphology was damaged, the tight connections between cells were damaged, the cell viability was weakened, and the paracellular permeability was increased after LPS treatment. Conclusions: The occurrence of sepsis is accompanied by intestinal barrier dysfunction. The level of miR-155 in septic intestinal barrier dysfunction is increased, and may participate in the occurrence and development of septic intestinal barrier dysfunction by promoting the release of inflammatory factors. The abnormal expression of miR-155 is of great value for the diagnosis and prognosis of early intestinal dysfunction in patients with sepsis, and can be used as an important indicator for the diagnosis and prognosis of early intestinal damage in sepsis. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Wildlife / Yesheng Dongwu Xuebao is the property of Chinese Journal of Wildlife Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the effect of miR-155 on the PI3K/Akt/mTOR signaling pathway in rheumatoid arthritis (RA) rats by targeting PIK3R1. Methods SD rats were randomly divided into control group, model group, miR-155 agomir group, miR-155 antagomir group, and miR-155 negative control group. RA model was induced in rats. After treatment with drugs, joint symptoms were observed. The arthritis index and hind toe volume were measured. HE staining was used to observe the pathological morphology of rat joint tissues. Levels of inflammatory factors IL-6, IL-17, and IL-18 in rat joint tissues was detected with the kits. PI3K/Akt/mTOR signaling pathway protein expression in rat joint tissues was detected with Western blotting. qRT-PCR experiment was used to detect the levels of miR-155 and PIK3R1 mRNA in rat joint tissues. Dual luciferase reporter gene experiment was used to detect the targeted regulation of miR-155 on PIK3R1. Results Compared to those in the control group, the symptoms of arthritis in the model group were obvious, the arthritis index, hind toe volume, joint tissue inflammatory factors IL-6, IL-17, and IL-18 levels, joint tissue p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR levels, joint tissue miR-155 level increased significantly (P<0.05), and the PIK3R1 mRNA level reduced significantly (P<0.05). Compared to those in the model group and the miR-155 negative control group, the above indexes of miR-155 antagomir group were significantly improved (P<0.05). The trend in miR-155 agomir group was opposite to that in miR-155 antagomir group (P<0.05). Conclusion MiR-155 targets to down-regulate the expression of PIK3R1, to activate PI3K/Akt/mTOR signal, to aggravate the joint damage of RA rats, and to down-regulate the expression of miR-155. It inhibits the activation of PI3K/Akt/mTOR signal and the occurrence and development of inflammation, and relieves the symptoms of arthritis. [ABSTRACT FROM AUTHOR]

Objective To investigate the role of miR-155 in the development and lung metastasis of osteosarcoma, and to explore its target proteins and related mechanisms. Methods We detected differential miR-155 expression in osteosarcoma and its lung metastasis process through relevant database analysis combined with qPCR detection of clinical tissue and cell samples. iTRAQ quantitative proteomics was used to screen the target protein of miR-155 in osteosarcoma and its lung metastasis. The selected miR-155 target protein was verified by Western blot in clinical tissue and cell samples. Results miR-155 expression was significantly higher in osteosarcoma tissue and lung metastatic tumor tissue than that in the control group. Compared with human normal osteoblasts, miR-155 expression in human osteosarcoma cell line was also significantly increased. A total of 3714 proteins were obtained by iTRAQ assay, and 253 differentially-expressed proteins were screened out, 144 of which were up-regulated and 109 were down-regulated. The prediction analysis and experiment verified that C/EBP β was a potential target protein of miR-155. Conclusion miR-155 expression is significantly increased in osteosarcoma and its lung metastasis process, and C/EBP β is a potential target of miR-155.

Objective To explore the effect of inhibiting miR-155 on cardiomyocyte apoptosis and inflammation in myocardial ischemia-reperfusion (MI/R) model. Methods Myocardial cells of H9c2 rats were divided into four groups: blank control group, myocardial ischemia-reperfusion group (MI/R group), negative control group and miR-155 inhibitor group. The expressions of miR-155, NF-κB signaling pathway related genes and Bax, Bcl-2 mRNA were detected by RT-qPCR. The contents of IL-8 and TNF-α were detected by ELISA. Western blot was used to detect the expression of NF-κB signaling pathway related genes and Bax, Bcl-2 protein. Results Compared with the control group, the expression of miR-155 in MI/R group was significantly increased (P＜0.05) while the expression of miR-155 in miR-155 inhibitor group was significantly decreased (P＜0.05). In MI/R group, the apoptosis rate, the content of IL-8 and TNF-α, the protein and mRNA expression of Bax and NF-κB signal pathway were significantly higher than those in the control group, while the protein and mRNA expression of Bcl-2 were lower (P＜0.05). After inhibition the expression of miR-155, the apoptosis rate, the content of IL-8 and TNF-α, the protein and mRNA expression level of Bax and NF-κB signal pathway related gene were significantly decreased, while the protein and mRNA expression by Bcl-2 were increased (P＜0.05). Conclusions Inhibition of miR-155 expression can protect MI/R injury through inhibition of apoptosis and inflammation. The potential mechanism is the inhibition of the activation of NF-κB signaling pathway.

Rejection has constantly been an unresolved challenge in the field of organ transplantation. The research on the mechanism of rejection plays a significant role in improving the efficacy of organ transplantation and enhancing the survival rate of graft. The innate and specific immune responses of the human body jointly participate in the graft rejection, leading to graft injury. In recent years, multiple researchers have conducted in-depth studies on the mechanism underlying the role of microRNA (miR) in regulating rejection. Among them, miR-155 has been widely considered as a key factor involved in immune regulation. The expression level and functional status of miR-155 may be intimately associated with the occurrence of rejection, which may become a new target for overcoming rejection. In this article, relevant studies on the role of miR-155 in regulating key immune cells in innate and specific immune responses were reviewed, aiming to provide novel ideas for the development of new immunosuppressants and rejection therapy. [ABSTRACT FROM AUTHOR]

Objective To preliminarily reveal the mechanism of miR-155 affects the sensitivity of colorectal cancer cells to 5-FU chemotherapy by targeting the expression level of TP53INP1. Method The human colorectal cancer cell line HCT116 was cultured, and the total RNA was extracted, then the reverse transcription system was constructed with miR-155 reverse transcription specific primer for PCR amplification, the expression of miR-155 in HCT116/Fu and HCT116 was detected by qRT PCR; Logarithmic growth cells were transfected with miR-155 mimics, miR-155 inhibitor and miR-155 negative control respectively, the effect of miR-155 on 5-FU drug sensitivity was detected by CCK-8 method, and the dual-luciferase reporter assay was used to verify the relationship between miR-155 and TP53INP1, the effect of miR-155 on the expression of TP53INP1 was detected by Western blot. Results The expression of miR-155 in HCT116/Fu cells was 7.25 times higher than that in HCT116 cells; At the same 5-FU Concentration, the rate of cell growth inhibition of HCT116+negative control was higher than that of HCT116+mimics, and the half inhibitory concentration was significantly lower than that of HCT116+mimics (P<0.05); TP53INP1 was the target gene of miR-155, which could significantly reduce the luciferase activity of wild-type TP53INP1 3'-UTR; After transfection of miR-155 mimics, the relative expression of TP53INP1 decreased significantly, and after transfection of miR-155 inhibitor, the relative expression of TP53INP1 increased significantly (all P<0.05). Conclusion The increased level of miR-155 decreased the sensitivity of HCT116 cells to 5-FU, miR-155 may affect the sensitivity of colorectal cancer cells to 5-FU by targeted regulating the expression level of TP53INP1. [ABSTRACT FROM AUTHOR]

Abstract: Objective To explore the relationship between the expression of miR-155 and programmed cell death 4 (PDCD4) in peripheral blood of infants with respiratory syncytial virus (RSV) bronchiolitis. Methods A total of 106 infants and young children with RSV bronchiolitis accepted by our hospital were collected as the research group. According to the severity of the disease, patients were separated into the mild group (n=36), the moderate group (n=41), and the severe group (n=29). Sixty-five infants who underwent physical examination in the child care clinic of our hospital were selected as the control group (n=55). The serum level of miR-155 in peripheral blood of infants and young children was measured by real-time quantitative PCR (qPCR) method. Levels of PDCD4, high sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α were measured by enzyme-linked immunosorbent assay (ELISA). The relationship between serum miR-155 and PDCD4 and their correlation with inflammatory factors in infants with RSV bronchiolitis were analyzed by Pearson correlation. Results Compared with the control group, the serum level of miR-155 was significantly increased in the study group, and the level of PDCD4 was significantly decreased (P＜0.05). In addition, the serum miR-155 level increased with the aggravation of the severity of RSV bronchiolitis, and the PDCD4 level reduced significantly (P＜ 0.05). Compared with the control group, serum levels of inflammatory factors hs-CRP, IL-6, IL-10 and TNF-α increased significantly in the study group (P＜0.05). Pearson correlation analysis showed that miR-155 and PDCD4 were negatively correlated (r=-0.790, P＜0.01), miR-155 was positively correlated with hs-CRP, IL-6, IL-10, and TNF-α (P＜0.01), and PDCD4 was negatively correlated with hs-CRP, IL-6, IL-10, and TNF-α (P＜0.01). Conclusion RSV bronchiolitis in infants and young children has abnormal expression of serum levels of miR-155 and PDCD4, and the two levels are negatively correlated. Serum levels of miR-155 and PDCD4 are tightly related to inflammatory factors. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To investigate the relationship between the expression of serum micro ribonucleic acid (miR)-34b-5p and miR-155 and the inflammatory factors and prognosis of premature infants with acute respiratory distress syndrome (ARDS). 92 premature infants with ARDS who were admitted to our hospital from February 2019 to March 2021 were selected, and they were divided into mild group (31 cases), moderate group (43 cases) and severe group (18 cases) according to the severity of ARDS, follow up the clinical outcome of children, according to the death in hospital, they were divided into survival group (51 cases) and death group (41 cases). The expressions of serum miR-34b-5p and miR-155, as well as interleukin-1 β(IL-1β), tumor necrosis factor -α(TNF-α) and interleukin- 6 (IL-6) in all the children were detected. The differences of the above indexes among the groups were compared, the correlation between the expressions of serum miR-34b-5p and miR-155 and inflammatory factors and the value of miR-34b-5p and miR-155 in predicting the prognosis of premature infants with ARDS were analyzed. The expression levels of serum miR-155 and the levels of IL-1β, TNF-αand IL-6 in the severe group were higher than those in the moderate group and mild group, and those in moderate group were higher than those in mild group (P<0.05). The expression level of serum miR-34b-5p in the severe group was lower than that in moderate and mild groups, and that in moderate group was lower than that in mild group (P<0.05). The expression level of serum miR-155 in the death group was higher than that in the survival group (P<0.05), and the expression level of miR-34b-5p in the death group was lower than those in the survival group (P<0.05). The expression level of miR-155 was positively correlated with the levels of IL-1β, TNF-αand IL-6 in premature infants with ARDS(P<0.05), and the expression level of miR-34b-5p was negatively correlated with the levels of IL-1β, TNF-αand IL-6(P<0.05). The area under curve(AUC) of miR-34b-5p and miR-155 predicting premature infant death in ARDS was 0.853, which was higher than 0.688 and 0.649 predicted by the two indexes alone. The expression levels of serum miR-34b-5p and miR-155 in premature infants with ARDS are related to the levels of serum inflammatory factors and prognosis, which can be used as potential indexes for condition evaluation and prognosis prediction of premature infants with ARDS. [ABSTRACT FROM AUTHOR]

The purpose of this study was to explore the relationship between dynamic enhancement of magnetic resonance, miR-27, miR-155 expression and breast cancer. One hundred breast cancer patients were selected as the observation group, and another 60 patients with benign breast lesions were selected as the control group. This study compared the two groups7 DCE-MRI quantitative parameters [transport constant (Ktrans), rate constant (Kep), extravascular intercellular space fraction (Ve)] and the expression of miR-27 and miR-155, and then performed correlation analysis to evaluate its diagnostic power. The expression levels of Ktrans, Kep, miR-27 and miR-155 in the observation group were higher than those in the control group (P<0.05). The expression levels of Ktrans and Kep in breast cancer patients were significantly positively correlated with the expression levels of miR-27 and miR-155 (P<0.05). Ktrans, Kep, miR-27 and miR-155 were independent influencing factors of breast cancer (P<0.05). The expression of KtranS, Kep, miR-27, miR-155 is related to histological grade, clinical stage, lymph node metastasis, progesterone and estrogen receptor expression (P<0.05). The AUC of the combined diagnosis of breast cancer by DCE-MRI quantitative parameters, miR-27, miR-155 expression is 0.905. DCE-MRI quantitative parameters (Ktrans, Kep) and the expression levels of miR-27 and miR-155 were up-regulated in breast cancer, and were related to pathological features. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exhaustive exercise leads to multiple redistribution of blood oxygen in the body, induces a strong inflammatory response, enhances the level of systemic inflammation, and damages kidney function. OBJECTIVE: To determine the effects of a single bout of exhaustive exercise on the expressions of renal NOD-like receptor protein 3 (NLRP3) inflammasome in rats and possible mechanism. METHODS: Twenty male Sprague-Dawley rats aged 3 months were randomly divided into a control group and an exhaustive exercise group, with 10 rats in each group. In the exhaustive exercise, three-level incremental exercise load treadmill training was performed to establish a one-time exhaustive exercise experimental animal model. No modeling was performed in the control group. Immediately after training, blood sample was collected from each rat, and then the kidney tissue was removed for hematoxylin-eosin staining to observe the morphological changes of renal cells. Renal thioredoxin-interacting protein (TXNIP), serum blood urea nitrogen, creatinine, creatine kinase, malondialdehyde, cystatin C and urine kidney injury molecule-1 levels were detected. Western blot was used to detect renal SIRT1, NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC) 1, Caspase-1 and interleukin-1β protein expression. RTqPCR was performed to detect serum and renal miR-155 and renal SIRT1 mRNA expression. Meanwhile, renal cell morphology was observed. RESULTS AND CONCLUSION: Compared with the control group, the levels of serum and renal miR-155 were significantly increased in the exhaustive exercise group (P < 0.01, P < 0.05). Compared with the control group, the protein and mRNA expression of renal SIRT1 was significantly decreased (both P < 0.01), while the protein expression of renal TXNIP, NLRP3, ASC-1, Caspase-1 and interleukin-1β was significantly increased in the exhaustive exercise group (P < 0.05 or 0.01). Moreover, the levels of serum blood urea nitrogen, creatinine, creatine kinase, malondialdehyde, cystatin C and urine kidney injury molecule-1 were significantly increased in the exhaustive exercise group compared with the control group (P < 0.05 or 0.01), and renal pathologic changes were aggravated. The expression of SIRT1 was negatively related to the protein expression of TXNIP and NLRP3 (r=-0.962, P < 0.01; r=-0.977, P < 0.01). The expression of miR-155 was negatively related to the protein expression of SIRT1 (r=-0.989, P < 0.01), and positively related to the protein expression of TXNIP and NLRP3 (r=0.902, P < 0.01; r=0.968, P < 0.05). Therefore, a single bout of exhaustive exercise increases the levels of serum and renal miR-155, reduces the expression of renal SIRT1 protein and mRNA, increases the expression of renal TXNIP, activates NLRP3 inflammasome, triggers inflammatory response and then aggravates the renal pathological damages, thereby impairing renal function. This may be one of the mechanisms of kidney injury induced by a single bout of exhaustive exercise. [ABSTRACT FROM AUTHOR]

目的 研究腔隙性脑梗死 (LI) 患者外周血 miR-155表达与血管新生因子缺氧诱导因子 -1α (HIF-1α), 血管内皮生长因子(VEGF) 的关系及对病情进展的预测价值。方法 选择2018年6月至2020年 12月在新郑市人民医院诊断为 LI的78例患者作为 LI 组,同期体检的90例健康志愿者作为对照组。检测两 组外周血 miR-155表达水平及血清 HIF-1α, VEGF 含量。采用入院时的简易智力状态检查量表评分评价 LI 组患者的认知功能,采用入院时及入院1周后美国国立卫生研究院卒中量表评分的变化评价 LI 组患者的病情 进展。结果 LI 组患者外周血 miR-155的表达水平高于对照组,差异有统计学意义(P<0.05)。LI组中重 度、中度认知功能障碍患者的外周血 miR-155表达水平高于认知功能正常患者,差异均有统计学意义 (P< 0.05) ;LI 组中外周血 miR-155 表达水平大于或等于中位数的患者和外周血 miR-155 表达水平低于中位数的 患者相比,血清 HIF-1α, VEGF 水平前者低于后者,差异均有统计学意义 (P<0.05);LI 组中病情进展患者的 外周血 miR-155 表达水平高于病情未进展患者,差异有统计学意义 (P<0.05)。受试者工作特征曲线分析证 实,外周血 miR-155对病情进展具有预测价值。结论 LI患者外周血 miR-155表达增加与血管新生因子 HIF1α 及 VEGF 减少, 病情进展有关,检测 miR-155 对病情进展具有预测价值。 [ABSTRACT FROM AUTHOR]

Objective To explore the dynamic expressions of serum miR-122 and miR-155 during the liver injury induced by valproate (VPA) in young mice and their relationship with liver injury. Methods Kunming mice aged 4 weeks were randomly divided into control groups (n=30) and experimental groups (n=56) according to random number table method. Seven experimental groups were given VPA 375 mg·kg-1 ·d-1 for 1 day, 3 days, 5 days, 7 days, 14 days, 21 days and 28 days consecutively. While five control groups were given 1 mL normal saline daily for 1 day, 7 days, 14 days, 21 days and 28 days. The serum samples and liver tissues of each group were collected. The pathological changes of liver tissue were observed by HE staining. The activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum were detected by automatic biochemical analyzer. The serum expression levels of miR-122 and miR-155 were detected by real-time quantitative polymerase chain reaction (qPCR). Results The histopathological results showed that liver cells had different degrees of vacuolar degeneration in the experimental groups. A small number of inflammatory cells were observed in the cytoplasm of hepatocytes on the day 3, 5, 7, a large number of hepatocytes were denatured and necrotic on day 21 and regenerated on day 28. It showed a trend of decreasing-increasing on ALT and AST. The expression level of miR-122 was down-regulated in the experimental group after administration, decreased to the lowest level on day 7 (decreased by 81%), and then up-regulated. However, the expression trend of miR-155 was opposite to that of miR-122, reached the peak on day 7, which was 2.88 times that of the control group. MiR-122 was positively correlated with ALT and AST (rs= 0.965 and 0.900, respectively, P＜0.05), while miR-155 was negatively correlated with AST (rs=-0.811, P＜0.05). Conclusion MiR-122 and miR-155 are involved in the occurrence of VPA drug-induced liver injury and are expected to become the early warning indicators. [ABSTRACT FROM AUTHOR]

This study explored the value of carotid ultrasound combined with CT and serum microRNA-124 (miR-124) and microRNA-155 (miR-155) in predicting the risk of secondary cerebral infarction in patients with carotid stenosis. Forty-three patients with carotid stenosis were selected as carotid stenosis group, and 43 normal volunteers were selected as normal group. The expression of miR-124 and miR-155 was detected by RT-PCR. Carotid artery stenosis was examined by carotid ultrasound. The blood vessels in the neck were examined by CT. The results showed that compared with the normal group, the expression of miR- 124 and miR-155 in carotid stenosis group was increased (P<0.05). Compared with ultrasound and CT, ultrasound combined with ct had higher accuracy and diagnostic value (P<0.05). It is found that carotid ultrasound, CT, miR-124 and miR-155 have high diagnostic value for carotid artery stenosis, and can be used to predict the risk of secondary cerebral infarction. [ABSTRACT FROM AUTHOR]

Objective To study the therapeutic effect of Liangxue Xiaoyin granule on psoriasis transgenic mice (K14- VEGF) and its effect on the miR-155/cytokine signal transduction inhibitor 1 (SOCS1) axis. Methods Eight untreated Swiss outbred line (FVB/NJ) mice were randomly selected as the control group. In addition, 24 SPF K14-VEGF transgenic mice were according to random number table method divided into model group, Liangxue Xiaoyin granule group and methotrexate group, 8 in each group. The control group and model group were intragastrically administered normal saline, Liangxue Xiaoyin granule group was intragastrically administered at a dose of 60 g/kg, methotrexate group was intragastrically administered at a dose of 2 mg/kg, once a day for 10 days. The severity index (PASI) score of psoriasis was observed, and the morphological changes of cells were observed by HE staining. The expression levels of serum TNF-α, IL23, IL-6 and IL-1 were detected by enzyme-linked immunosorbent assay (ELISA). The real-time fluorescence quantitative analysis (qPCR) was used to detect the expression of miR-155, and the expression of SOCS1 protein was determined by Western blot (WB) assay. Results Compared with the control group, the model group showed spinous layer thickening and superficial dermal lymphocyte infiltration. Compared with the model group, the pathological severity of mice decreased significantly, and the cell morphology recovered in the Liangxue Xiaoyin granule group and the methotrexate group. Compared with the control group, the PASI score, the expression levels of TNF- α, IL-23, IL-6, IL-1 and miR-155 were significantly higher, the expression level of SOCS1 was decreased significantly in the model group (P < 0.05). Compared with model group, the PASI score, the expression levels of TNF-α, IL-23, IL-6, IL-1 and miR-155 were decreased significantly in Liangxue Xiaoyin granule group and methotrexate group (P < 0.05), and the expression level of SOCS1 was significantly higher (P < 0.05). There was no significant difference between Liangxue Xiaoyin granule group and methotrexate group (P＞0.05). Conclusion Liangxue Xiaoyin granule may alleviate the inflammatory reaction and alleviate the symptoms of psoriasis transgenic mice by inhibiting the activation of the miR-155/SOCS1 axis. [ABSTRACT FROM AUTHOR]

To investigate and analyze the mechanism of miR-155 targeting pten-pi3kakt pathway to promote the proliferation and inhibit the apoptosis of nasopharyngeal carcinoma cells. 105 healthy adult SD male rats were selected as research objects, and they were divided into observation group and control group and experimental group by random draw method, with 35 rats in each group. The rat model of nasopharyngeal carcinoma was established by subcutaneous injection of cancer inducer dimethylenitropiperazine in the axils and progenitor phopol. The observation group was given mir-155 inhibitor intervention, the experimental group was given PI3K inhibitor intervention, and the control group was not given any intervention. The relative expressions of mir-155 were detected by real-time fluorescence quantitative PCR, the expressions of PTEN, PI3K and p-akt were detected by immunohistochemistry, and the expression levels of bcl-2, Bax and Ezrin were detected by Western blot. The three groups of rats were compared and the correlation was analyzed. The relative expression levels of mir-155 in the experimental group, the observation group and the control group were (34.88± 1.32), (29.72± 1.23) and (35.01± 1.34), respectively, which were significantly lower in the observation group than in the experimental group and the control group (F=23.105, P=0.000). The expression rate of PTEN in experimental group, observation group and control group increased gradually, while the expression rate of PI3K and p-akt decreased gradually (all P<0.05). Pearson correlation analysis showed that the relative expression level of miR-155 in nasopharyngeal carcinoma rats was positively correlated with the expression rate of PTEN, but negatively correlated with the expression rate of PI3K and p-akt (all P<0.05). The expression levels of bcl-2 and Ezrin in the experimental group, the observation group and the control group showed a trend of gradual increase, while the expression levels of Bax protein showed a trend of gradual decrease. Moreover, one-way anova showed that there were significant differences among the groups (all P<0.05). MiR-155 may play a role in promoting the proliferation of nasopharyngeal carcinoma cells and inhibiting the apoptosis of nasopharyngeal carcinoma cells by targeting the pten-pi3kakt signaling pathway. It may be a new target in the treatment of nasopharyngeal carcinoma. [ABSTRACT FROM AUTHOR]

BACKGROUND: Currently, studies have focused on the role and mechanism of nuclear factor-kappa B pathway in the pathological process of acute lung injury in burned rats, such as the targeting inhibition of κB kinase by miR-155, which further weakens the activity of nuclear factor-κB and plays a role in acute lung injury in burned rats. However, there are still some pathological mechanisms to be studied and confirmed. OBJECTIVE: To investigate the effect of miR-155 on acute lung injury in burned rats through nuclear factor-κB pathway. METHODS: The rat models of acute lung injury were established by warm water bath simulating bum injury. The burned rats were divided into acute lung injury, miR-155-mimics and miR-155-inhibitor groups. After fluid resuscitation, the rats in the miR-155-mimics and miR-155-inhibitor groups were injected into the tail vein of 5 µL of miR-155-mimics and miR-155-inhibitions, respectively. The expression levels of tumor necrosis factor-a and interleukin-1β in bronchoalveolar lavage fluid were detected by ELISA. The lung morphology in the three groups was observed by hematoxylin-eosin staining. The protein expression levels of nuclear factor-KB and cyclooxygenase 2 were evaluated by western blot assay. The nuclear factor-κB protein in lung tissues was detected by immunohistochemistry. RESULTS AND CONCLUSION: (1) The results of hematoxylin-eosin staining showed that the severity of lung injury in the miR-155-inhibitor group, acute lung injury group and the miR-155-mimics group was increased gradually (P < 0.05). (2) ELISA results showed that compared with the acute lung injury group, the expression levels of tumor necrosis factor-a and interleukin-1β were increased in the miR-155-mimics group (P < 0.05). and decreased in the miR-155-inhibitorgroup (P< 0.05). (3) Western blot assay results showed that compared with the acute lung injury group, the expression levels of nuclear factor-κB and cyclooxygenase 2 proteins were increased in the miR-155-rnimics group (P < 0.05), and decreased in the miR-155-inhibitorgroup (P< 0.05). (4) lmmunohistochemical results showed that the expression level of nuclear factor-κB was increased in the miR-155-inhibitor group, which was dark brown. The expression of nuclear factor-κB in cytoplasm and nucleus of neutrophils, mononuclear macrophages, alveolar epithelial cells was the most obvious. (5) These results indicate that in lung tissue cells, decreased miR-155 can down-regulate nuclear factor-κB activity, which reduces the inflammatory response of the lung between the damaged tissue. [ABSTRACT FROM AUTHOR]

Objective: To establish a intervertebral disc degeneration of nucleus pulposus cell line (NP) with stable overexpression of miR-155, and to explore the effect and mechanism of miR-155 in apoptosis of NP. Methods: The lentivirus expression vector was first constructed and the recombinant lentivirus was rescued in 293T cells. Then the stable overexpression cell lines were obtained by infecting the degenerated nucleus pulposus cells of the intervertebral disc. At the same time the empty vector and the blank cell group were set up as controls. The expression of lentivirus label protein GFP was observed by fluorescence microscope. The total RNA was extracted respectively from three groups of cells and the expression of miR-155 was detected by RT-qPCR method. Apoptosis of cells was detected by flow cytometry and the expression of apoptosis-related proteins (FADD, Caspase-3, Bcl-2 and Bax) was detected by Western-Blot. The change of cell mitochondrial membrane potential was detected with the JC-1 kit. Results: Using fluorescence microscope, green fluorescence was observed in the over-expressed cell lines and empty vector cell lines infected by lentivirus, but green fluorescence was not found in the blank cell group. RT-qPCR results showed that the expression of miR-155 in stable overexpression cell line (GV369-miR-155-NP) was highly higher than that in empty vector cell line and blank cell control group (P<0.05). Compared with the empty vector group (GV369-NP) and the blank cell control group, the apoptosis rate of overexpressed group (GV369-miR-155-NP) was significantly lower (P<0.05). The expressions of FADD, caspase-3 and Bax were significantly decreased, while the expression of bcl-2 was significantly increased (P<0.05). Conclusions: MiR-155 may inhibit the apoptosis of degenerative nucleus pulposus cells through preventing FasL-Fas pathway targeting Caspase-3 and FADD or mitochondrial pathway. [ABSTRACT FROM AUTHOR]

ObjectiveTo study the different expression of miR-155 in glioblastoma stem-like cells(GSCs), neural stem cells(NSCs) and different grades glioma. To clarify the relationship of miR-155 expression, degree of malignancy and prognosis of glioma patients. MethodsGSCs and NSCs were isolated in vitro using neurosphere culture, then characteristics of the GSCs and NSCs were identified by experiments of immunoflurescence and xenograft. QRT PCR technology was used to detect the expression levels of miR-155 in GSCs, NSCs, gliomas of different grades and normal brain tissues. Kaplan-meier survival curve analysis was performed in combination with patient prognosis. ResultsThe expression of miR-155 increased significantly in GSCs compared with NSCs（P＜0.05）, and also increased with the malignant degree of glioma.The expression level of miR-155 in malignant glioma(WHO III, IV) was obviously higher than that of normal brain tissue(all P<0.05). The high expression of miR-155 was closely related to the poor prognosis of glioma. ConclusionThe expression of miR-155 elevates in GSCs and malignant glioma specimens, and can be considered as biomarker for diagnosis and prognosis judgment of glioma. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects and the mechanism of action of microRNA-155(miR-155) on proliferation,invasion and migration of osteosarcoma Saos2 cells. Methods: The expression of miR-155 in normal osteoblasts and osteosarcoma Saos2 cells was detected by real-time PCR, and the transfection efficiency of miR-155-mimic and miR-155-inhibitor was measured by qRT-PCR. CCK-8 assay was used to evaluate the cell proliferation. Transwell assay and wound healing assay were used to detect the invasion and migration ability of Saos2 cells, respectively. SOCS1 and p-STAT3 protein expression was examined by using western blot assay. Dual luciferase reporter gene assay was performed to determine the target gene. Results: The expression of miR-155 was significantly higher in osteosarcoma Saos2 cells than normal osteoblasts(P <0.001). After transfection with miR-155-mimic or miR-155-inhibitor, miR-155 expression of Saos2 cells was significantly upregulated or downregulated, respectively(P <0.001).Overexpression of miR-155 promoted proliferation, invasion and migration of Saos2 cells, and decreased the protein level of SOCS1, as well as increased the phosphorylation level of STAT3. The difference was statistically significant(P<0.05). Conversely, downregulation of miR-155 inhibited the proliferation, invasion, and migration of Saos2 cells. The difference was statistically significant(P <0.05).Conclusion: miR-155, which is highly expressed in osteosarcoma Saos2 cells, can activate the STAT3 signaling pathway by inhibiting the expression of SOCS1, thereby promotes cell proliferation, migration and invasion. Therefore, targeting miR-155 therapy may be a potential approach for osteosarcoma. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of microRNA-155 (niiR-155) in the invasion potential of colon cancer cell and the exact underlying mechanism. Methods: The expression level of miR-15 5 in colon cancer and adjacent normal tissues was detected by realtime quantitative PCR(RT-PCR). niiR-155 mimics (niiR-155). or siRNA against β-catenin (β-catenin siRNA) were transfected into human colon cancer cell line SW-480 respectively using Upofectamine 2000, and RT-PCR was used to measure the niRNA expression levels of niiR-155 and β-catenin. and β-catenin protein expression level was detected by Western blot. The in-vitro cell invasion ability was determined by Transwell invasion assays after up-regulating miR-155 or knocking down of β-catenin. Results: The expression levels of niiR-155 was higher in colon cancer tissue compared to adjacent normal tissues. niiR-155 directly up-regulates the niRKA and protein expression lewis of β-catenin In addition, niiR-155 enhances cell invasion abilities, whereas the invasion potentiality was decreased after co-treated withβ-catenin siRNA. Conclusions: niiR-155 promotes the invasion potential of colon cancer cell, at least partly through the upregulation of p-catenin. The findings of mis study suggest mat niiR-155 and β-catenin may have a unique potential as a novel biomarker candidate for diagnosis and treatment in tumor metastasis. [ABSTRACT FROM AUTHOR]

Objective To investigate the expression changes of miR-155 during the 3-oxo-C12-HSL inhibition of maturation of human monocyte-derived dendritic cells( Mo-DCs). Methods Human peripheral blood CD14+monocytes were isolated and induced into Mo-DCs by recombinant human granulocyte-mononuclear colony-stimulating factor and recombinant human interleukin-4. Immature Mo-DCs were divided into the negative control group,model group,experimental group 1,and experimental group 2. The negative control group was added with the same volume of PBS,the model group was added with LPS( 1 μg/m L),the experimental group 1 was added with LPS( final concentration of 1 μg/m L) and 3-oxo-C12-HSL with a final concentration of 50 μmol/L,the experimental group 2 was added with LPS( 1 μg/m L) and 3-oxo-C12-HSL with a final concentration of 100 μmol/L for 48 h. The phenotypes( CD80,CD40,CD11 c,and HLA-DR)of Mo-DCs in each group were detected by flow cytometry. The levels of cytokines( IL-12 and IL-10) in the cell culture supermatants were detected by enzyme-linked immunosorbent assay. The expression of miR-155 was detected by real-time fluorescent quantitative PCR. Results Compared with the negative control group,the expression of CD80,CD40,and HLA-DR in the model group was higher,the IL-10 level was lower,the IL-12 level was higher,and the expression of miR-155 was higher( P 0. 05). When we compared the experimental group 1 and experimental group 2 with the model group,as well as experimental group 2 with experimental group 1,the expression of CD80,CD40,and HLA-DR was lower,the IL-10 level was higher,the IL-12 level was lower,and the miR-155 expression was lower( all P 0. 05). Conclusion The expression of miR-155 during the 3-oxo-C12-HSL inhibition of maturation of Mo-DCs is decreased,suggesting that 3-OC12-HSL may inhibit the maturation of Mo-DCs by reducing the expression of miR-155. [ABSTRACT FROM AUTHOR]

Objective To explore the mechanism of microRNA (miRNA, miR)-155 in the rejection after liver transplantation in rats. Methods The rats were divided into two groups. In the xenograft model group (rejection group, n=10), the donors were male Lewis rats and the recipients were male BN rats. In the allograft model group (control group, n=10), both the donors and recipients were male Lewis rats. The rat models with orthotopic liver transplantation were established by two-cuff technique in two groups. At postoperative 7 d, the animals were sacrificed for the collection of blood and liver tissue samples. The serum levels of alanine aminotransferase (ALT), total bilirubin (TB), and cytokines of interleukin (IL)-2, IL-4, interferon (IFN)-γ were quantitatively measured. The pathological changes of liver tissues were observed under light microscope. In each group, three liver tissue samples were prepared and subject to highthroughput sequencing. The miRNAs related to rejection were identified for bioinformatics analysis to predict and analyze relevant signaling pathways and genes. Results In the rejection group, the serum levels of ALT and TB were significantly higher than those in the control group (both P<0.01). Compared with the control group, the levels of IL-2 and IFN-γ were considerably up-regulated (both P<0.01), whereas the level of IL-4 was dramatically down-regulated (P<0.01). Pathological examination demonstrated that more evident rejections were observed in the rejection group than the control group. High-throughput sequencing revealed that the expression level of miR-155 was significantly up-regulated in the rejection group, which was 5.89 times of that in the control group. Bioinformatics analysis demonstrated that up-regulation of miR-155 was associated with the mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK) and T cell receptor signaling pathways. The genes which were probably responsible for regulation included the yeast autophagy related gene 1(ATG1) and its homologous gene ULK2, insulin-like growth factor-1 (Igf-1) and G proteincoupled receptor regulatory gene (Arrb1), etc. Conclusions miR-155 might promote the incidence and progression of rejection after liver transplantation in rats. The involved signaling pathways probably include the mTOR, MAPK signaling pathway and T cell receptor signaling pathway. ATG1, ULK2, Igf-1, and Arrb1 genes may participate in this process. [ABSTRACT FROM AUTHOR]

Background and objective Despite undergoing curative resection, the 5-year survival rate for stage III non-small cell lung cancer (NSCLC) patients is less than 25%. There is a need for biomarkers for prediction of survival and guiding individual therapy. MiR-155 is one of most commonly upregulated miRNAs in malignancies, and regulates multiple pro-oncogenic pathways. We aimed to investigate the prognostic impact of miR-155 in resected stage III NSCLC patients. Methods Tumor formalin-fixed, paraffin-embedded (FFPE) from 162 resected stage III NSCLC patients were collected. Total RNA including miRNA was extracted, and qRT-PCR was used to determine the expression of miR-155. Results Spearman rank correlation test showed a positive correlation between miR-155 expression and nodal status (r=0.169, P=0.032). MiR-155 expression had a significant prognostic impact in the total cohort (P

Objective · To investigate serum miR-155 expression in patients with chronic kidney disease (CKD) and to explore whether miR-155 influences epithelial-mesenchymal transition (EMT) in renal tubular epithelial cells via down-regulating Krüppel-like factor 4 (KLF4). Methods · Serum samples from 126 CKD Ⅰ stage patients, 163 CKD Ⅲ stage patients, and 170 healthy individuals were collected. RT-PCR was used to test the serum miR-155 expression. In cell experiment, EMT in renal tubular epithelial cells was induced with 10 μg/L TGF-β. miR-155 mimic and miR-NC were transfected to renal tubular epithelial cells cultured in vitro. Changes in cell morphology were observed with optical microscope. Transwell assay was used to test the cell migration ability. Western blotting was used to examine the expressions of SMα-actin, Collagen Ⅰ, Collagen Ⅳ, E-cadherin, and KLF4. Bioinformatics predicted that the potential target gene for miR-155 was KLF4, which was confirmed with luciferase assay. Plasmids with over-expressed KLF4 were transfected to renal tubular epithelial cells and expressions of SMα-actin, collagen Ⅰ, collagen Ⅳ, E-cadherin, and KLF4 were detected. Results · CKD Ⅲ stage patients had lower serum miR-155 expression compared with healthy individuals and CKD Ⅰ stage patients. In cell experiment, the expression of SMα-actin, collagen Ⅰ, collagen Ⅳ and KLF4 renal tubular epithelial cells decreased and the expression of E-cadherin increased after being transfected with miR-155 mimic, as compared with the control group. Results of the luciferase assay showed that miR-155 significantly decreased the luciferase activity of KLF4-3'-UTR plasmid. Expressions of SMα-actin, collagen Ⅰ, and collagen Ⅳ in renal tubular epithelial cells were increased and the expression E-cadherin was decreased after being transfected with plasmids with over-expressed KLF4. Conclusion · CKD patients have low serum miR-155 expression. miR-155 can inhibit EMT in renal tubular epithelial cells by down-regulating KLF4. [ABSTRACT FROM AUTHOR]

Objective: To study the effects of miR-155 on the cell cycle of prostate cancer and the underlying mechanisms. Methods: The cell cycles of DU145 and PC-3 cells were evaluated after anti-miR-155 transfection by FACS. p53 and p21 expression were evaluated by western blot and RT-PCR. Results: The cell cycle of DU145 and PC-3 cells were down regulated obviously after anti-miR-155 transfection(P<0.05), and the protein and mRNA expression of p53 and p21 were obviously increased (P<0.01). In addition, the protein and mRNA expression of CDK2 and cyclin E were also decreased obviously (P<0.01). Conclusions: Inhibition of miR-155 could modulate the cell cycles of DU145 and PC-3 cells in vitro by p53/p21 pathways and by down regulating the expression of CDK2 and cyclin E. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expressions of miR-155 and miR-203 in the lesional skin and adjacent non-lesional skin of psoriatic patients. Methods: Biopsies were carried out on 12 psoriatic patient donors to obtain lesional skin and adjacent nonlesinal skin which were made into FFPE samples. In situ hybridization was performed on tissue slides using 5' and 3' DIG-labeled detection probes to localize the expression of miR-155 and miR-203. SYBR Green Ⅰreal-time PCR were carried out to compare the abundance of miR-155 and miR-203 between lesional and nonlesinal psoriatic skin. Results: The expression of miR-155 in lesional skin was significantly higher than that of nonlesional skin in all 12 pairs of sample while the expression of miR-203 showed no significant difference between the lesional and nonlesional samples. Mi R-155 expressed in both epidermis and dermis, which was higher in basal cell layer and localized in nucleus. miR-203 expression was higher in basal cell layer and the lower part of epidermis, expressed in both nucleus and cytoplasm. Conclusion: Mi R-155 located in the cell nucleus of both epidermis and dermis and its expression in lesional skin was dramatically elevated in comparison to the nonlesional skin, implying its role in the pathogenesis of psoriasis. [ABSTRACT FROM AUTHOR]

Objective To determine association between the expression of miR-155, miR-16, miR-25 and miR-133 and epidermal growth factor receptor (EGFR) in lung adenocarcinoma (ADC) samples of non-smoking female, and their clinical significance thereof. Methods According to EGFR types, 112 non-smoking female ADC patients were divided into two groups: EGFR wild (n=51) and EGFR mutant (n=61) groups. Expression levels of four miRNAs were detected by real time quantitative PCR. T-test was used to compare differences of four miRNAs expression in two groups. ADC patients were divided into high miRNA expression group and low expression group according to the mean value of miRNAs expression. Logrank test was used to compare the survival difference between the two subgroups. Cox proportional hazards regression analysis was performed to determine the association between different ages (≤60，>60), EGFR types, miRNAs expression and overall survival. Results The expression of miR-25 was significantly higher in EGFR mutant group than that in EGFR wild group (P < 0.05). There were no significant differences in the survival rates of patients with different ages, EGFR types, and the expressions of miR-155, miR-16 and miR-133a. Patients with the lower expression of miR-25 had the higher survival time than patients with the higher expression of miR-25 (P < 0.05). In EGFR mutation group, there was no relationship between four miRNAs and the prognosis of ADC (P > 0.05). In EGFR wild group, the lower expression of miR-16, miR-25 or miR-133a was associated with longer survival in ADC (P < 0.05). Cox proportional hazards regression analysis revealed that the high expression of miR-25 was an independent risk factor for non-smoking female patients with ADC (P < 0.05). Conclusion miR-25 is an independent prognostic indicator for non-smoking female patients with ADC. High expression of miR-25 is found in non-smoking female patients with ADC, particularly in patients with EGFR wild-type, which may suggest a poor prognosis. [ABSTRACT FROM AUTHOR]

Objective To investigate the role and mechanism of miR-155 in invasion and metastasis of lung adenocarcinoma A549 cells. Methods Real-time PCR and fluorescence in situ hybridization were used to detect the miR-155 expression in patients' lung adenocarcinoma and adjacent tissue and lymph nodes. Scratch test and Transwell migration assay were used to assess the effect of miR-155 on the A549 cell migration and invasion capability. Bioinformatics software was used to predict the target genes of miR-155, and using luciferase to assay the target gene. Western blot and real-time PCR were performed to confirm the role of miR-155 expression in the regulation of target gene PTEN. Results The real-time quantitative PCR showed that the miR-155 expression levels in adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were 4.1±0.5, 9.6±3.1 and 7.8±2.2, respectively. The in situ hybridization showed that the expression rates of miR-155 in the adjacent normal tissue, lung adenocarcinoma and metastatic lymph nodes were (23.2±15.3)%, (75.4±20.2)% and (60.4±25.1)%, respectively. The Scratch assay showed that the wound healing rates in the miR-155 mimics group, miR-155 mimics NC group, miR-155 inhibitor group and miR-155 inhibitor NC group at 24 h were (43.2±2.2)%, (21.3±4.2)%, (24.3±5.3)%, and (35.2±5.1)%, and that at 48 h were (75.2±4.5)%, (52.6±5.2)%, (39.4±4.2)%, and (51.5±4.3)%, respectively. Dual luciferase reporter gene assay showed that the value of the luciferase in the miR-155 mimics group co-transfected with PTEN 3'UTR-containing wild-type and mutant plasmids were 4.7±0.5 and 7.3±0.7, and the miR-155 mimics luciferase values of the control group co-transfected with PTEN 3'UTR-containing wild-type and mutant plasmids were 7.8±0.9 and 7.5±0.8, respectively. The real-time quantitative fluorescence PCR showed that the relative expression of PTEN protein in the miR-155 mimics group, miR-155 mimics control group, miR-155 mimics inhibitor group, and miR-155 inhibitor control group were 0.5±0.3, 1.0±0.1, 2.2±0.2 and 1.2±0.1, respectively. The Western blot assay detected that the relative expression of PTEN protein levels in the miR-155 mimics group, miR-155 mimics control group, miR-155 inhibitor group and miR-155 inhibitor control group were 0.4±0.1, 1.0±0.3, 2.8±0.2 and 1.4±0.1, respectively. The differences in PTEN mRNA and protein expressions of the four groups were statistically significant (P<0.05 for all). Conclusions miR-155 may promote the invasion and metastasis of lung adenocarcinoma through reducing the target PTEN gene expression. [ABSTRACT FROM AUTHOR]

Objective: To investigate the expressions and significances of miR-21 and miR-155 in peripheral blood B cells of patients with systemic lupus erythematosus (SLE). Methods: 93 cases of patients with SLE were divided into mild active group (n=49) and moderate and severe active group (n=44) according to SLEDAL scores. 40 healthy were selected as the control group. The expressions of miR-21, miR-155, bone morphogenetic protein-2 (BMP-2) and bone morphogenetic protein receptor Ⅱ(BMPRⅡ) in peripheral blood B cells were detected by using real-time quantitative PCR. Results: The relative expressions of miR-21 and miR-155 in peripheral blood B cells of SLE patients were higher than the control group (P<0.05). The relative expressions of miR-21 and miR-155 in peripheral blood B cells in the moderate and severe active group were higher than the mild active group and the control group, and the mild active group was higher than the control group, the differences were statistically significant (P<0.05). The relative expressions of BMP-2 mRNA and BMPRⅡ mRNA in peripheral blood B cells of SLE patients were higher than the control group (P<0.05). The relative expressions of BMP-2 mRNA and BMPRⅡ mRNA in peripheral blood B cells in moderate and severe active group were higher than the mild active group and the control group, and the mild active group was higher than the control group, the differences were statistically significant (P<0.05). Pearson correlation analysis showed, the relative expressions of miR-21 and miR-155 in peripheral blood B cells of the SLE patients were positively correlated with BMP-2 mRNA and BMPR Ⅱ mRNA (r=0.292, 0.365 and 0.481, 0.279, P<0.05), the relative expressions of miR-21 and miR-155 in peripheral blood B cells of the SLE patients were negatively correlated with the levels of complement C3 and C4 (r=-0.570,-0.289 and-0.751,-0.308, P<0.05). Conclusion: MiR-21 and miR-155 were highly expressed in the peripheral blood B cells of SLE patients, which might play a role by the abnormal activation of BMP signaling and were negatively correlated with the complement C3 and C4. they might expected to be indicators in monitoring the patient's condition. [ABSTRACT FROM AUTHOR]