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Hyperlipidemia is a common metabolic disorder that can lead to cardiovascular disease. PDK4 is a key enzyme that regulates glucose and fatty acid metabolism and homeostasis. The aim of this study is to explore the correlation between PDK4 expression and dyslipidemia in obese children, and to find new therapeutic targets for hyperlipidemia in children. The expression of PDK4 in serum was detected by qRT-PCR. Receiver operating characteristic curve was used to analyze the relationship between PDK4 and dyslipidemia. Upstream miRNAs of PDK4 were predicted by the database and verified by dual luciferase reporter gene assay and detected by qRT-PCR. The hyperlipidemia mouse model was established by high-fat diet (HFD) feeding, and the metabolic disorders of mice were detected. PDK4 is poorly expressed in the serum of obese children. The upstream of PDK4 may be inhibited by miR-107, miR-27a-3p, and miR-106b-5p, which are highly expressed in the serum of obese children. Overexpression of PDK4 improves lipid metabolism in HFD mice. miR-27a-3p silencing upregulates PDK4 to improve lipid metabolism. In conclusion, PDK4 has a diagnostic effect on dyslipidemia in children, while lipid metabolism in hyperlipidemic mice could be mitigated by upregulation of PDK4, which was inhibited by miR-107, miR-27a-3p and miR-106b-5p on upstream. [ABSTRACT FROM AUTHOR]

Alzheimer’s disease (AD) is an ultimately fatal, degenerative brain disease in the elderly people. In the current work, we assessed the defensive capability of isovitexin (IVX) through an intracerebroventricular injection of streptozotocin (STZ)-induced AD mouse model.

Lung cancer causes over 1.6 million mortalities worldwide annually. MicroRNAs (miRs) are involved in various types of cancer-associated processes. The present study investigated the possible mechanism of miR-107 in the development of lung cancer in order to identify novel targets for clinical treatment. The expression levels of miR-107 and its putative target gene TP53 regulated inhibitor of apoptosis 1 (TRIAP1) were measured in lung cancer tumor tissues and non-tumor adjacent tissues. Subsequently, the association between TRIAP1 and miR-107 was investigated using a dual-luciferase reporter assay. Following transfection, the effects of miR-107 and TRIAP1 on the proliferation and apoptosis of lung cancer cell lines in vitro were investigated using Cell Counting Kit-8 and flow cytometry assays, respectively. Furthermore, the regulatory effect of miR-107 on the expression levels of TRIAP1 and associated proteins was analyzed using a western blot assay. The results revealed lower expression levels of miR-107 and higher expression levels of TRIAP1 in lung cancer tumor tissues compared with non-tumor adjacent tissues. The dual-luciferase reporter assay demonstrated that TRIAP1 is a target gene of miR-107. Additionally, the results revealed that overexpression of miR-107 resulted in a lower proliferation rate and higher apoptosis rate of A549 cells, compared with the negative control (NC) and control groups (P<0.01). The variation of cell proliferation and apoptosis induced by miR-107 mimics was reversed by co-transfection with pcDNA3.1-TRIAP1. Furthermore, the expression levels of cyclin D1 and proliferating cell nuclear antigen were markedly decreased in the miR-107 mimics group compared with the NC group (P<0.01). The expression levels of BCL2 associated X apoptosis regulator, tumor protein p53 and caspase 3 were upregulated and the expression levels of TRIAP1 and BCL2 apoptosis regulator were significantly reduced in the miR-107 mimics group compared with the NC group (P<0.01). The results of the present study suggested that miR-107 regulates lung cancer cell proliferation and apoptosis by targeting TRIAP1. [ABSTRACT FROM AUTHOR]

Background: ‒ Alzheimer’s disease (AD) is an ultimately fatal, degenerative brain disease in the elderly people. In the current work, we assessed the defensive capability of isovitexin (IVX) through an intracerebroventricular injection of streptozotocin (STZ)-induced AD mouse model. Methods: ‒ Mice were separated into four cohorts: sham-operated control mice; STZ-intoxicated Alzheimer’s mice; IVX cohort, IVX + STZ; and Ant-107 cohort, antagomiR-107 + IVX/STZ as in the IVX cohort. Results: ‒ The outcomes indicated that IVX administration ameliorated spatial memory loss and blunted a cascade of neuro-noxious episodes – including increased amyloid-beta (Aβ) and degraded myelin basic protein burden, neuroinflammation (represented by elevated caspase-1, TNF-α and IL-6 levels) and autophagic dysfunction (represented by altered LC3-II, Atg7 and beclin-1 expressions) – via the inhibition of PI3K/Akt/ mTOR signalling axis. We considered the question of whether the epigenetic role of microRNA-107 (miR-107) has any impact on these events, by using antagomiR-107. Conclusion: ‒ This probing underscored that miR-107 could be a pivotal regulatory button in the activation of molecular signals linked with the beneficial autophagic process and anti-inflammatory activities in relation to IVX treatment. Hence, this report exemplifies that IVX could guard against Aβ toxicity and serve as an effectual treatment for patients afflicted with AD. [ABSTRACT FROM AUTHOR]

The role of long intergenic noncoding RNA 00893 (Linc00893) in asthenozoospermia (AS) and its impact on sperm motility remains unclear The present study explored the effect of Linc00893 on AS, specifically its effect on sperm motility and its relationship with spermatogonial stem cell (SSC) vitality and myosin heavy chain 9 (MYH9) protein expression. Linc00893 expression was analyzed in semen samples using reverse transcription-quantitative PCR, revealing a significant downregulation in samples from individuals with AS compared with those from healthy subjects. This downregulation was found to be negatively correlated with parameters of sperm motility. To further understand the role of Linc00893, small interfering RNA was used to knockdown its expression in SSCs. This knockdown led to a marked decrease in cell vitality and an increase in apoptosis. Notably, Linc00893 knockdown was shown to inhibit MYH9 expression by competitively binding with microRNA-107, a finding verified by dual-luciferase reporter and RNA immunoprecipitation assays. Furthermore, using the GSE160749 dataset from the Gene Expression Omnibus database, it was revealed that MYH9 protein expression was downregulated in AS samples. Subsequently, lentiviral vectors were constructed to induce overexpression of MYH9, which in turn reduced SSC apoptosis and counteracted the apoptosis triggered by Linc00893 knockdown. In conclusion, the present study identified the role of Linc00893 in AS, particularly its regulatory impact on sperm motility, SSC vitality and MYH9 expression. These findings may provide information on the potential regulatory mechanisms in AS development, and identify Linc00893 and MYH9 as possible targets for diagnosing and treating AS-related disorders. [ABSTRACT FROM AUTHOR]

Abstract Background Although previous studies have shown promise for targeting Musashi RNA-binding protein 2 (MSI-2) in diverse tumors, the role and mechanism of MSI-2 for cervical cancer (CC) progression and the regulation of MSI-2 expression remains unclear. Methods Using gene expression and bioinformatic analysis, together with gain- and loss-of-function assays, we identified MSI-2 as a novel oncogenic driver and a poor prognostic marker in CC. We explored the regulation of c-FOS by MSI-2 via RNA-immunoprecipitation and luciferase assay, and confirmed a direct inhibition of MSI-2 by miR-143/miR-107 using luciferase assay. We assessed the effect of a natural antibiotic Mithramycin A on p53, miR-143/miR-107 and MSI-2 expression in CC cells. Results MSI-2 mRNA is highly expressed in CC tissues and its overexpression correlates with lower overall survival. MSI-2 promotes CC cell growth, invasiveness and sphere formation through directly binding to c-FOS mRNA and by increasing c-FOS protein expression. Furthermore, miR-143/miR-107 are two tumor suppressor miRNAs that directly bind and inhibit MSI-2 expression in CC cells, and downregulation of miR-143/miR-107 associates with poor patient prognosis. Importantly, we found that p53 decreases the expression of MSI-2 through elevating miR-143/miR-107 levels, and treatment with a natural antibiotic Mithramycin A increased p53 and miR-143/miR-107 expression and reduced MSI-2 expression, resulting in the inhibition of CC cell proliferation, invasion and sphere formation. Conclusions These results suggest that MSI-2 plays a crucial role in promoting the aggressive phenotypes of CC cells, and restoration of miR-143/miR-107 by Mithramycin A via activation of p53 may represent a novel therapeutic approach for CC.

The aim of the present study was to investigate the mechanism of microRNA (miR)-107 in targeting regulator of G-protein signaling 4 (RGS4) in hepatic carcinoma. SK-HEP-1 cells were transfected with miR-107 mimics and control mimics. Reverse transcription-quantitative PCR was performed to determine the miR-107 expression levels, and following miR-107 upregulation, MTT, colony formation, transwell and wound-healing assays were performed to assess cell proliferation, colony-forming ability, invasion and migration, respectively. In addition, the effect of miR-107 upregulation on the cell cycle and apoptosis in SK-HEP-1 cells was evaluated using flow cytometry. Western blot analysis was performed to measure the protein expression levels of RGS4, epidermal growth factor receptor (EGFR), CXC chemokine receptor type 4 (CXCR4) and matrix metalloproteinase (MMP)-2 and −9. Expression level changes and the association between miR-107 and RGS4 in HCC cells were assessed using dual luciferase analysis. The results indicated that the overexpression of miR-107 in HCC cells suppressed cellular proliferation, invasion, migration and colony-forming ability, but promoted apoptosis and G1 phase arrest. Furthermore, miR-107 mimics notably increased the protein expression level of RGS4, but significantly downregulated that of EGFR, CXCR4 and MMP-2 and −9. Together, these findings suggest that targeting this potential mechanism of miR-107 may be beneficial in the treatment of patients with HCC. [ABSTRACT FROM AUTHOR]

Objective: Apelin, an adipocytokine, is up-regulated by insulin and suppresses pancreatic insulin secretion. One of the key microRNAs in insulin resistance caused by obesity, is microRNA-107. MicroRNA-375 is expressed in the pancreatic islet cells. We aimed to explore apelin-13 and micro- RNA-107 and 375 in obese women with type 2 diabetes (T2D). Materials and Methods: Fifty obese women with newly diagnosed T2D and 50 non-diabetic obese women, as controls, were selected. Quantitative PCR and ELISA were used to measure the expression of microRNA-107 and 375 and Apelin-13 concentration, respectively. The role of apelin-13 was investigated in an in vitro model. Apoptosis was evaluated by flow cytometry. Results: Apelin-13 levels in diabetics were significantly more than controls (p = 0.012). The expressions of micro- RNA-107 and 375 of diabetic group were increased, in comparison to the control group. There was no correlation between apelin-13 and microRNA-107 and 375 in diabetic and control groups. Significant correlations between apelin-13 and serotonin (p < 0.001) and estimated average glucose (p < 0.02) and insulin (p < 0.03) were only observed in the diabetic group. Conclusion: Serum levels of apelin-13 and circulating microRNA-107 and 375 could be used as biomarkers for diabetes, particularly in obese subjects. However, more study is needed in this field. [ABSTRACT FROM AUTHOR]

Previous studies have reported that miR-107 could be utilized as a potential peripheral biomarker in prostate cancer (PCa). However, the specific functions of miR-107 in prostate cancer and its relevant mechanisms are still unknown. The aim of this research was to investigate the cellular functions of miR-107 in PCa and reveal the relevant mechanisms. MicroRNA tailing quantitative real-time PCR (qRT-PCR) was adopted to measure the expression of miR-107 in PCa cell line DU145 and PC3, as well as in normal prostate cell line RWPE-1. The miR-107 expression pattern in PCa tissues and paired peritumoral tissues were determined by Chromogenic In Situ Hybridization (CISH). Cell viability, colony formation, flow cytometry cell cycle and apoptosis, wound healing and Transwell migration assays were performed to study the miR-107 functions in PCa cells. Further, qRT-PCR, western blot analysis and dual-luciferase reporter assays were conducted to verify the target of miR-107 in PCa. Results demonstrated that miR-107 was downregulated in PCa cells and tissues in comparison with normal prostate cells and peritumoral tissues, and the over-expression of miR-107 suppressed proliferation and induced G1/S arrest of PCa cells but had no effects on apoptosis or cell motility of PCa cells. MiR-107 was found to target cyclin E1 (CCNE1) in PCa cells by directly binding to its 3'-UTR. In conclusion, miR-107 could be a potential tumor suppressor in PCa, and the restoration of miR-107 might provide a new therapeutic option for PCa. [ABSTRACT FROM AUTHOR]

Coronary atherosclerosis is a long‐term, sustained, and evolving inflammatory disease manifested with the remodeling of the coronary arteries. The purpose of this study is to explore the potential role of microRNA‐107 (miR‐107) in vascular endothelial cells (VECs) in coronary atherosclerosis by regulating the KRT1 gene and the Notch signaling pathway. A mouse model of coronary atherosclerosis was established. The relationship between miR‐107 and KRT1 was analyzed and verified by dual‐luciferase reporter assay. The functional role of miR‐107 in coronary atherosclerosis was determined using ectopic expression and depletion. Blood lipid levels and atherosclerotic index (AI) were measured in atherosclerotic mice. Expression pattern of miR‐107, KRT1, Notch signaling pathway, inflammatory/anti‐inflammatory factors, and endoplasmic reticulum (ER) stress‐related genes was evaluated by means of reverse transcription quantitative polymerase chain reaction, western blot analysis, and enzyme‐linked immunosorbent assay. Meanwhile, cell‐cycle distribution and cell apoptosis in VECs were assessed by flow cytometry. Atherosclerotic mice exhibited higher blood lipid levels, AI, apoptotic index, and KRT1‐positive expression as well as inhibited Notch signaling pathway when compared with normal mice. The miR‐107 was revealed to bind to KRT1; miR‐107 upregulation or KRT1 silencing resulted in reductions in blood lipid levels and AI, inhibition in cell apoptosis, inflammation, and ER stress. Restored miR‐107 or downregulated KRT1 activated the Notch signaling pathway. These results supported the notion that miR‐107‐targeted KRT1 inhibition activated the Notch pathway, thereby, protecting against the coronary atherosclerosis. Findings in this study might provide a novel biomarker for the coronary atherosclerosis treatment. These results supported the notion that miR‐107‐targeted KRT1 inhibition activated Notch pathway, thereby, protecting against coronary atherosclerosis. Findings in this study might provide a novel biomarker for coronary atherosclerosis treatment. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are endogenous non-coding RNAs implicated in atherosclerosis. The aim of the present study was to explore the function of circRNA-0044073 in atherosclerosis. Reverse transcription quantitative polymerase chain reaction assays were used to measure the expression levels of circRNA-0044073, microRNA (miRNA/miR)-107, janus kinase 1 (JAK1), signal transducer and activator of transcription 3 (STAT3), B-cell lymphoma 2 (Bcl-2) and v-myc avian myelocytomatosis viral oncogene homolog (c-myc) in in blood cells from patients with atherosclerosis. RNA pull-down and luciferase reporter assays were then used to determine the association between circRNA and miR expression, and miR and gene expression, respectively. Matrigel invasion assay and flow cytometry were used to analyze cell invasion and cell cycle. Western blot analysis and ELISA were used to evaluate the expression levels of proteins. It was identified that the expression of circRNA-0044073 was upregulated and the expression of miR-107 was downregulated in atherosclerotic blood cells. Overexpression of circRNA-0044073 promoted the proliferation of human vascular smooth muscle cells (HUVSMCs) and human vascular endothelial cells (HUVECs), while overexpression of miR-107 inhibited their proliferation. In addition, circRNA-0044073 suppressed the levels of miR-107 via a sponge mechanism. Lipopolysaccharide (LPS) affected the proliferation of HUVSMCs and HUVECs, and also resulted in changes in circRNA-0044073 expression levels. CircRNA-0044073 promoted the proliferation and invasion of HUVSMCs and HUVECs in spite of the opposite effect observed with LPS treatment. The JAK/STAT signaling pathway was activated in patients with atherosclerosis. CircRNA-0044073 favored the activation of the JAK/STAT signaling pathway and inflammation in HUVSMCs and HUVECs. These data indicate that circRNA-0044073 is upregulated in atherosclerosis and promotes the proliferation and invasion of cells by targeting miR-107 and activating the JAK/STAT signaling pathway, potentially offering a target for novel treatment strategies against atherosclerosis. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is a common malignant tumor with high global increase and mortality. While Skullcapflavone I has been reported to exert anti-tumor effect in several cancers, its role in CRC has not previously been investigated. Recent studies have also demonstrated that microRNA-107 (miR-107) and tropomyosin alpha-1 (TPM1) are important regulators of cancer cell proliferation, but it remains unclear if these are involved in regulating the effect of Skullcapflavone I on CRC cells. This study therefore assessed the effects of Skullcapflavone I on CRC cell proliferation and investigated miR-107 and TPM1 regulatory effects on this process. The results showed that Skullcapflavone I significantly suppressed cell proliferation and viability and down-regulated PCNA and Cyclin D1protein levels. It also down-regulated miR-107 expression which then promoted TPM1 expression, but miR-107 over-expression abolished Skullcapflavone I anti-proliferative effects. Furthermore, Skullcapflavone I inhibited the activations of MEK/ERK and NF-κB signal pathway activation by regulating TPM1 in HCT116 cells. These results demonstrated that Skullcapflavone I increased the expression of TPM1 by downregulating miR-107 and inhibiting the MEK/ERK and NF-κB signal pathways. It then inhibited HCT116 cell proliferation, and therefore Skullcapflavone I may provide new methodology in colorectal cancer treatment. [ABSTRACT FROM AUTHOR]

Accumulation of senescent endothelial cells can contribute to endothelium dysfunction. Suppression of MTOR signaling has been shown to delay senescence but the mechanism that underpins this effect, particularly one that involves miRNAs, remains to be further defined. This study sought to identify miRNAs involved in MTORC1-mediated inhibition of replicative senescence in endothelial cells. Pre-senescent HUVECs were prolonged treated with low dose rapamycin (1 nM), an MTOR inhibitor. Rapamycin treatment down-regulated the phosphorylated MTOR, RPS6 and 4EBP1 expressions, which confirmed MTORC1 suppression. Prolonged low dose rapamycin treatment has significantly reduced the percentage of senescence-associated beta galactosidase (SA-β gal) positively stained senescent cells and P16INK4A expression in these cells. On the contrary, the percentage of BrdU-labelled proliferating cells has significantly increased. RPTOR, a positive regulator of MTORC1 was knockdown using RPTOR siRNA to inhibit MTORC1 activation. RPTOR knockdown was evidenced by significant suppressions of RPTOR mRNA and protein expression levels. In these cells, the expression of miR-107 was down-regulated whereas miR-145-5p and miR-217 were up-regulated. Target gene prediction revealed PTEN as the target of miR-107 and this was confirmed by biotin pull-down assay. Over-expression of miR-107 has decreased PTEN expression, increased MTORC1 activity, induced cell cycle arrest at G0/G1 phase and up-regulated P16INK4A expression but mitigated tube formation. Collectively, our findings revealed that delayed endothelial replicative senescence caused by the inhibition of MTORC1 activation could be modulated by miR-107 via its influence on PTEN. [ABSTRACT FROM AUTHOR]

The homemade production of carbon screen-printed electrodes (C-SPEs) with a three‑carbon electrode system is reported, along with its application in electrochemical sensing. It is highlighted herein as main novelty that a simple carbon ink may be employed in the preparation of the 3-electrode system, including the pseudo-reference electrode, thereby avoiding the addition of silver or other suitable metal and simplify the construction of such devices, reducing costs and time. Screen-printed technology was employed to produce the 3-electrodes and the corresponding electrical paths. This was achieved by the manual application of a commercial carbon ink into a polyvinyl chloride (PVC) substrate allowing the production of > 20 SPEs. The optimization of the SPE assembly was made by univariate mode, until the best electrical features of the electrode-solution interface were achieved. Several electrochemical techniques were used for this purpose, namely cyclic voltammetry (CV), square wave voltammetry (SWV) and electrochemical impedance spectroscopy (EIS). Raman Spectroscopy and Thermogravimetric Analysis (TGA) were also used for materials and electrode surface characterization. The usefulness of such devices was tested by modifying the working electrode with a sensing layer for microRNA-107, a potential biomarker in Alzheimer's Disease (AD). For this purpose, the surface was functionalized with carboxylic groups, activated by carbodiimide reaction and bound to a suitable oligonucleotide probe containing the complementary sequence. Finally, the microRNA-107 sequence hybridized with its probe, proving the efficiency of the C-SPEs in electrochemical sensing. Overall, this study brings into light the possibility of preparing simple homemade electrodes with a 3‑carbon electrode system that stands out by the low cost, disposability and versatility of the presented platform, holding a great potential for application in point-of-care devices using electrochemical sensing. [ABSTRACT FROM AUTHOR]

The increase of vascular wall tension can lead to endothelial injury during hypertension, but its potential mechanism remains to be studied. Our results of previous study showed that HUVECs could induce changes in HMGB1/RAGE to resist abnormal mechanical environments in pathological mechanical stretching. In this study, we applied two different kinds of mechanical tension to endothelial cells using the in vitro mechanical loading system FlexCell-5000T and focused on exploring the expression of miR-107 related pathways in HUVECs with excessive mechanical tension. The results showed that miR-107 negatively regulated the expression of the HMGB1/RAGE axis under excessive mechanical tension. Excessive mechanical stretching reduced the expression of miR-107 in HUVECs, and increased the expression of the HMGB1/RAGE axis. When miR-107 analog was transfected into HUVECs with lipo3000 reagent, the overexpression of miR-107 slowed down the increase of the HMGB1/RAGE axis caused by excessive mechanical stretching. At the same time, the overexpression of miR-107 inhibited the proliferation and migration of HUVECs to a certain extent. On the contrary, when miR-107 was silent, the proliferation and migration of HUVECs showed an upward trend. In addition, the study also showed that under excessive mechanical tension, miR-107 could regulate the expression of FGF-2 by HMGB1. In conclusion, these findings suggest that pathological mechanical stretching promote resistance to abnormal mechanical stimulation on HUVECs through miR-107/HMGB1/RAGE/FGF-2 pathway, thus promote vascular repair after endothelial injury. The suggest that miR-107 is a potential therapeutic target for hypertension. Schematic illustration of the role of the miR-107/HMGB1/RAGE/FGF-2 axis after hypertensive-induced excessive mechanical stretching leads to cellular injury. [Display omitted] • Excessive mechanical stretching of blood vessels during hypertension causes endothelial damage. • The miR-107/HMGB1/RAGE axis promotes endothelial repair by promoting FGF-2 expression. • The protein interaction between HMGB1 and FGF-2 was confirmed by immunoprecipitation. • GO enrichment showed that HMGB1/RAGE/FGF-2 actively responded to extracellular stimuli. [ABSTRACT FROM AUTHOR]

The disruption of blood-brain barrier (BBB) and endothelial cell dysfunction, associated with the cerebrovascular deposition of the amyloid-beta (Abeta) protein, have been characterized as the key pathological characteristics in Alzheimer's disease (AD). In various biologic processes of AD, researchers have proven that mircroRNAs (miRNAs) play critical roles. However, the role and function of miRNAs in the disruption of BBB of AD still remain unclear. Here, we found that mircroRNA-107 (miR-107) is endogenously expressed in human brain microvascular endothelial cells (ECs) of BBB model, while it is significantly down-regulated in ECs pre-incubated with Abeta. Abeta significantly impairs the integrity, increases the permeability of BBB, inhibits the viability of endothelial cells (ECs), and meanwhile down-regulates the expression of tight junction proteins ZO-1, Occludin and Claudin-5. Overexpression of miR-107 largely abrogated Abeta-induced disruption of BBB and endothelial cell dysfunction. Furthermore, overexpression of miR-107 also down-regulates endophilin-1, which is involved in the regulation of BBB permeability and the expression of ZO-1, Occludin, and Claudin-5. Both bioinformatics and luciferase reporter assays demonstrated that Endophilin-1 was a direct and functional downstream target of miR-107. In conclusion, our results indicate that overexpression of miR-107 is able to prevent Abeta-induced blood-brain barrier disruption and endothelial cell dysfunction by targeting endophilin-1. [ABSTRACT FROM AUTHOR]

Cervical cancer is among the most prevalent forms of cancer worldwide. C-C chemokine receptor type 5 (CCR5) is hypothesized to be a key functional protein involved in tumorigenesis. However, the role of CCR5 in cervical cancer remains unclear. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to evaluate the mRNA and protein expression levels of CCR5 in human cervical carcinoma tissues. Furthermore, a small interfering RNA was employed to knockdown CCR5 in HeLa and C33A cells. MTT, colony formation and Transwell assays were performed to determine the effects of this knockdown on cell viability, proliferation and invasion. In addition, micro RNA (miR)-107 was identified as a potential candidate regulator of CCR5 using miR prediction algorithms, and the effects of miR-107 and its antisense miR on CCR5 mRNA expression were determined. The results of the present study indicated that CCR5 is overexpressed in human cervical cancer tissues compared with adjacent normal tissues, and its downregulation inhibits cervical cancer cell growth and proliferation. Furthermore, the downregulation of CCR5 appears to suppress cervical cancer cell invasion. Finally, the tumor suppressor miR-107 was able to directly target CCR5 and inhibit its expression. These results suggest that the upregulation of CCR5, which is inhibited by miR-107, may play a carcinogenic role in cervical cancer and could provide a novel therapeutic target in the future. [ABSTRACT FROM AUTHOR]

The expression level of microRNA-107 (miR-107) has been proved to be decreased in many human malignant cancers. Especially in glioma, accumulating evidence indicates that miR-107 may play important parts in cell proliferation, apoptosis, and invasion in glioma. However, its clinical significance in glioma has not been investigated. This study aims at investigating the relationship between miR-107 expression level and clinical significance and analyzing its value of miR-107 in valuing the prognosis of glioma patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure the expression of miR-107 in 80 glioma and 17 normal brain tissues. The results showed the miR-107 expression level in glioma tissues was significantly lower than those in normal brain tissues ( p < 0.001). The decreased expression of miR-107 in glioma was positively associated with high WHO grade ( p < 0.001), low Karnofsky performance score (KPS) ( p < 0.001), and large tumor size ( p < 0.001) and had a significant impact on overall survival (OS) ( p < 0.001) and progression-free survival (PFS) ( p < 0.001) according to Kaplan-Meier survival with log-rank test. Finally, Cox regression analyses showed that low miR-107 expression ( p < 0.001) might be an independent prognostic parameter to predict poor prognosis. In conclusion, it is the first data to prove that expression level of miR-107 may be a novel and valuable prognostic factor in glioma. [ABSTRACT FROM AUTHOR]

Highlights: [•] Correlation between miR-107 expression levels and clinicopathological factors in patients with gastric cancer. [•] Identification of miR-107 as a transcriptional target of NF-κB. [•] Overexpression of miR-107 promotes gastric cancer cell proliferation. [•] miR-107 regulates expression of cell-cycle regulators, miR-107 antisense reduces the proliferation of gastric cancer cells and miR-107 negatively regulates FOXO1 expression in gastric cancer cells. [ABSTRACT FROM AUTHOR]

[Display omitted] • Hypoxia decreases lncRNA H19 expression in NSCs. • LncRNA H19 overexpression attenuates hypoxia-induced NSCs injury. • LncRNA H19 knockdown promotes hypoxia-induced NSCs injury. • LncRNA H19 overexpression activates Wnt/β-catenin and PI3K/AKT pathways. • LncRNA H19 overexpression affects NSCs properties by reducing miR-107 expression. Neonatal hypoxia-ischemia (HI) is one of the commonest conditions which seriously influences the development of infants' nervous system and causes series of neurological sequelaes. The aim of the present study was to analyze the potential regulatory mechanism of long non-coding (lnc) RNA H19 under hypoxia conditions. Neural stem cells (NSCs) were incubated in hypoxic conditions for 8 h to induce hypoxia injury. qRT-PCR was performed to detect H19 or micro (miR)-107 expression. Cell Counting Kit-8 (CCK-8) assay and Annexin V-FITC/PI staining assay were employed to detect the effects of hypoxia on cell viability and apoptosis, respectively. Moreover, NSCs were transfected with H19 overexpressing plasmid or shRNA-H19 and then subjected to hypoxia treatment. The effects of H19/miR-107 on NSC cell biological behaviors were confirmed. Furthermore, the signaling pathways involved in HI were analyzed using western blot. Hypoxia treatment restrained cell viability and induced cell apoptosis in NSCs. Overexpression of lncRNA H19 attenuated hypoxia-induced NSCs injury, while knockdown of lncRNA H19 aggravated NSCs injury. Further experiments suggested that miR-107 up-regulation reversed the effects of lncRNA H19 overexpression on NSCs. Moreover, the activation of Wnt/β-catenin and PI3K/AKT pathways triggered by H19 were reversed by miR-107 up-regulation in hypoxia-treated NSCs. LncRNA H19 overexpression attenuated hypoxia-induced NSCs injury and promoted activation of Wnt/β-catenin and PI3K/AKT pathways through downregulating miR-107. [ABSTRACT FROM AUTHOR]

Colorectal cancer is one of the most common cancers in the world. This study aimed to investigate the correlation between microRNA-107 (miR-107) expression level and the prognosis in colorectal cancer patients with its clinical significance. 80 cases of cancer tissues and 15 cases of adjacent cancer tissues were collected from colorectal cancer patients treated with surgery from February 2006 to January 2010. The expression of miR-107 was detected by real-time PCR. The correlation between miR-107 expression and clinic pathological factors and survival time of patients was statistically analyzed. The expression level of miR-107 in cancer tissues (0.0213 ± 0.0096) was significantly higher than that in adjacent tissues (0.0355 ± 0.0487). The expressions of miR-107 in patients with different TNM stages, Dukes stages, and lymph node metastasis rates were significantly different (P < 0.05). Cox proportional hazards regression model showed that miR-107 may be an independent factor affecting the prognosis of colorectal cancer patients (P < 0.05). The hazard ratio (HR) was 5.165. MiR-107 is highly expressed in colorectal cancer tissues and is closely related to the pathogenesis, progression, and metastasis of colorectal cancer. MiR-107 is expected to become a new molecular marker to assist the diagnosis, treatment effect and prognosis evaluation of colorectal cancer, and may also become a new target for colorectal cancer biotherapy., Competing Interests: None., (IJCEP Copyright © 2020.)

Background/aim: Patients with advanced non-small cell lung cancer (NSCLC) frequently face a dismal prognosis because of lack of curative therapies. We, therefore, conducted a preclinical investigation of the therapeutic efficacy of microRNA-107 (miR-107)., Materials and Methods: The effects of miR-107 on cell proliferation and target gene expression were studied. Combinatorial effects of miR-107 and parthenolide were evaluated., Results: Cell proliferation was repressed in A549 NSCLC cells transfected with miR-107. Inhibitor of nuclear factor kappa B kinase subunit gamma was directly targeted by miR-107. Overexpression of miR-107 in A549 cells sensitized them to parthenolide along with a marked reduction of cyclin-dependent kinase 2., Conclusion: Our findings unveil an important biological function of miR-107 in regulating lung cancer cell proliferation and elevating an antiproliferative effect of parthenolide on lung cancer cells, suggesting that miR-107 could be beneficial benefit treatment for advanced NSCLC., (Copyright© 2018, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)

Background: Although previous studies have shown promise for targeting Musashi RNA-binding protein 2 (MSI-2) in diverse tumors, the role and mechanism of MSI-2 for cervical cancer (CC) progression and the regulation of MSI-2 expression remains unclear., Methods: Using gene expression and bioinformatic analysis, together with gain- and loss-of-function assays, we identified MSI-2 as a novel oncogenic driver and a poor prognostic marker in CC. We explored the regulation of c-FOS by MSI-2 via RNA-immunoprecipitation and luciferase assay, and confirmed a direct inhibition of MSI-2 by miR-143/miR-107 using luciferase assay. We assessed the effect of a natural antibiotic Mithramycin A on p53, miR-143/miR-107 and MSI-2 expression in CC cells., Results: MSI-2 mRNA is highly expressed in CC tissues and its overexpression correlates with lower overall survival. MSI-2 promotes CC cell growth, invasiveness and sphere formation through directly binding to c-FOS mRNA and by increasing c-FOS protein expression. Furthermore, miR-143/miR-107 are two tumor suppressor miRNAs that directly bind and inhibit MSI-2 expression in CC cells, and downregulation of miR-143/miR-107 associates with poor patient prognosis. Importantly, we found that p53 decreases the expression of MSI-2 through elevating miR-143/miR-107 levels, and treatment with a natural antibiotic Mithramycin A increased p53 and miR-143/miR-107 expression and reduced MSI-2 expression, resulting in the inhibition of CC cell proliferation, invasion and sphere formation., Conclusions: These results suggest that MSI-2 plays a crucial role in promoting the aggressive phenotypes of CC cells, and restoration of miR-143/miR-107 by Mithramycin A via activation of p53 may represent a novel therapeutic approach for CC.

The aim of this study is to elucidate whether and how miR-107 participates in the modulation of paclitaxel sensitivity in non small cell lung cancer (NSCLC). By qRT-PCR, we found that miR-107 is significantly down-regulated in paclitaxel-resistant A549/Taxol cells compared with corresponding paclitaxel-sensitive counterparts. Overexpression of miR-107 suppresses paclitaxel resistance of A549/Taxol cells through directly inhibiting Bcl-w. Overexpression of miR-107 promotes apoptosis and inhibits proliferation and mobility of A549/Taxol cells under treatment with paclitaxel in vitro . Moreover, miR-107 inhibits in vivo paclitaxel resistance in xenograft model. MiR-107/Bcl-w axis regulates paclitaxel chemoresistance through PI3K-Akt pathway. Our results suggest that up-regulation of miR-107 resensitizes paclitaxel-resistant NSCLC cells by targeting Bcl-w, which reveals a potential mechanism of miR-107 in reversing drug resistance., Competing Interests: None.

Cervical cancer is among the most prevalent forms of cancer worldwide. C-C chemokine receptor type 5 (CCR5) is hypothesized to be a key functional protein involved in tumorigenesis. However, the role of CCR5 in cervical cancer remains unclear. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to evaluate the mRNA and protein expression levels of CCR5 in human cervical carcinoma tissues. Furthermore, a small interfering RNA was employed to knockdown CCR5 in HeLa and C33A cells. MTT, colony formation and Transwell assays were performed to determine the effects of this knockdown on cell viability, proliferation and invasion. In addition, micro RNA (miR)-107 was identified as a potential candidate regulator of CCR5 using miR prediction algorithms, and the effects of miR-107 and its antisense miR on CCR5 mRNA expression were determined. The results of the present study indicated that CCR5 is overexpressed in human cervical cancer tissues compared with adjacent normal tissues, and its downregulation inhibits cervical cancer cell growth and proliferation. Furthermore, the downregulation of CCR5 appears to suppress cervical cancer cell invasion. Finally, the tumor suppressor miR-107 was able to directly target CCR5 and inhibit its expression. These results suggest that the upregulation of CCR5, which is inhibited by miR-107, may play a carcinogenic role in cervical cancer and could provide a novel therapeutic target in the future.

MicroRNAs (miRNAs) are dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC). MiR-107 has been implicated in several types of cancer regulation; however, relatively little is known about miR-107 in human HCC. In the present study, we showed that the overexpression of miR-107 accelerates the tumor progression of HCC in vitro and in vivo through its new target gene, CPEB3. Furthermore, our results demonstrated that CPEB3 is a newly discovered tumor suppressor that acts via the EGFR pathway. Therefore, our study demonstrates that the newly discovered miR-107/CPEB3/EGFR axis plays an important role in HCC progression and might represent a new potential therapeutic target for HCC treatment.

Background: MicroRNAs (miRNAs) are small, non-coding RNAs which can function as oncogenes or tumor suppressor genes in human cancers. Researchers have found that the expression level of miR-107 was decreased in human non-small cell lung cancer (NSCLC) tissues and cell lines, however, its clinicopathological and prognostic significance in NSCLC has not been investigated., Methods: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of miR-107 in 137 pairs of fresh NSCLC and matched adjacent normal tissue specimens. The chi-square test and Fishers exact tests were used to examine the associations between miR-107 expression and the clinicopathological characters. The overall survival (OS) and progression-free survival (PFS) were analyzed by log-rank test, and survival curves were plotted according to Kaplan-Meier., Results: The expression level of miR-107 was significantly lower in tumor tissues than that in corresponding noncancerous tissues (0.4676 ± 0.2078 vs. 1.000 ± 0.3953, P<0.001). Low expression of miR-107 was found to significantly correlate with TNM stage (p=0.001), regional lymph node involvement (p=0.04), and tumor differentiation (p=0.003). Kaplan-Meier analysis with the log-rank test indicated that low miR-107 expression had a significant impact on OS (35.2% vs. 69.3%; P=0.008) and PFS (30.0% vs. 56.2%; P=0.029). In a multivariate Cox model, we found that miR-107 expression was an independent poor prognostic factor for both 5-year OS (HR=2.57, 95% CI: 1.88-10.28; P=0.007) and 5-year PFS (HR=3.08, 95% CI: 2.01-8.92; P=0.003)., Conclusion: The expression of miR-107 was decreased in NSCLC. Low expression of miR-107 was significantly associated with tumor progression and decreased survival in patients with NSCLC, indicating that miR-107 may serve as a novel prognostic marker in NSCLC.