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Objective To investigate the effects of lncRNA-MEG3 knockdown on the proliferation, apoptosis, clonal formation, cell cycle, and to analyze the targeted relationship between lncRNA-MEG3 and miR-93 in human uterine leiomyoma (UL) cell line. Methods Human UL cell line SK-UT-1 was cultured in vitro, and the cells were divided into lncRNA-MEG3 knockdown group and negative control group; the lncRNA-MEG3 knockdown plasmid and negative control plasmid were transfected into cells of the two groups, respectively. The expression of lncRNA-MEG3 and miR-93 in the cells was detected by qRT-PCR, the proliferation activity was detected by CCK8 assay, the clonal formation ability was detected by plate colony formation assay, the cell cycle and apoptosis rate were detected by flow cytometry, and the expression levels of proliferation-related proteins (Ki67, PCNA), apoptosis-related proteins (Bax, Bcl-2), and Wnt/β-catenin pathway-related proteins (Wnt3a, β-catenin) were detected by Western blotting. The targeted relationship between lncRNA-MEG3 and miR-93 was verified by dual luciferase reporter gene assay. Results Compared with the negative control group, the expression of lncRNA-MEG3 decreased, the expression of miR-93 increased, the OD values decreased at 48, 72, and 96 h, the number of clonal formation was reduced, the proportion of cells in the G0/G1 phase increased, the proportion of cells in the G2/M phase decreased, the apoptosis rate increased, the expression of Wnt3a, β-catenin, Ki67, PCNA, Bcl-2 decreased, and the expression of Bax increased in the lncRNA-MEG3 knockdown group (all P<0. 05). LncRNA-MEG3 could target miR-93 to reduce the relative luciferase activity (P<0. 05). Conclusions Knocking down lncRNA-MEG3 can inhibit the proliferation, colony formation, and Wnt/β-catenin pathway of UL cells, block the cell cycle in G0/G1 phase, and induce apoptosis, thereby inhibiting the growth of UL cells. There is a targeted relationship between lncRNA-MEG3 and miR-93. [ABSTRACT FROM AUTHOR]

Objective：This study aims to examine the expression of ZBTB3 in human glioblastoma (GBM) tissues and cell lines, and to explore the effects of ZBTB3 on the proliferation and clonal formation of GBM cells and their regulatory mechanism. Methods：The expression of ZBTB3 in tumor tissues of GBM patients was analyzed by GEPIA2 database. The mRNA and protein expression levels of ZBTB3 in GBM cell lines (U251, U373, U87) were detected by RT⁃PCR, qPCR and Western blot, and U87 cell line was identified with the highest expression of ZBTB3. CCK ⁃ 8 and clonal formation assay were used to examine the effects of silencing ZBTB3 on the proliferation and clonal formation of U87 cells. U87 cells were treated with p38MAPK, AMPK and Akt1 inhibitors, and the phosphorylation levels of p38MAPK, AMPK and Akt1 were detected by Western blot. ZBTB3 mRNA and protein levels were detected by RT ⁃ PCR, qPCR and Western blot. Cell proliferation and clone formation were examined by CCK ⁃ 8 and clone formation assay. Results：The expression of ZBTB3 in tumor tissues of GBM patients was significantly higher than that in normal tissues. The expression levels of ZBTB3 in U251, U373 and U87 cell lines were examined, and the highest expression in U87 cells was observed. Silencing ZBTB3 markedly inhibited the proliferation and clonal formation of U87 cells. AMPK inhibition could not only obviously reduce the expression level of ZBTB3 in U87 cells, but also markedly attenuate the proliferation and clonal formation of U87 cells. Conclusion：The expression of ZBTB3 is obviously increased in GBM tissues and cells, and the AMPK ⁃ up ⁃ regulated ZBTB3 expression promotes the proliferation and clonal formation of GBM cells. [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.)

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.)

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.)

Objective: Multiple myeloma (MM) is caused by abnormal cloning of plasma cells. miR-184 is abnormally expressed in several types of tumors, but its expression and role in MM have not been reported., Methods: The bone marrow samples of healthy controls and MM patients were collected, and plasma cells were sorted. The multiple myeloma cell line OPM-2 was cultured and assigned into miR-NC+siRNA-NC group, miR-184 inhibitor+siRNA-NC group, and miR-184 inhibitor+siRNA-Notch1 group. Cell proliferation was assessed by MTT assay. Clone formation was evaluated by colony formation assay. Cell apoptosis activity was tested with flow cytometry. Notch1 and cleaved caspase3 protein expressions were detected., Results: MiR-184 expression was increased in myeloma plasma cells ( P <0.05). Transfection of miR-184 inhibitor can downregulate miR-184 expression, increase the levels of Notch1 and cleaved caspase3, inhibit OPM-2 cell proliferation, restrain colony formation, enhance caspase3 activity, and suppress tumor cell invasion ( P <0.05). However, administration of siRNA-Notch1 retarded the effect of miR-184 inhibitor by decreasing the expressions of Notch1 and cleaved caspase3, enhancing colony formation and tumor cell invasion, as well as inhibiting caspase3 activity and cell proliferation., Conclusion: Our data indicated that miR-184 expression is increased in myeloma plasma cells. Down-regulation of miR-184 promotes MM cell apoptosis and inhibits proliferation and colony formation by regulating Notch1 expression., (© 2024 by the Association of Clinical Scientists, Inc.)

Background: Hepatocellular carcinoma (HCC) is a primary contributor to cancer-related mortality on a global scale. However, the underlying molecular mechanisms are still poorly understood. Long noncoding RNAs are emerging markers for HCC diagnosis, prognosis, and therapeutic target. No study of LINC01767 in HCC was published., Aim: To conduct a multi-omics analysis to explore the roles of LINC01767 in HCC for the first time., Methods: DESeq2 Package was used to analyze different gene expressions. Receiver operating characteristic curves assessed the diagnostic performance. Kaplan-Meier univariate and Cox multivariate analyses were used to perform survival analysis. The least absolute shrinkage and selection operator (LASSO)-Cox was used to identify the prediction model. Subsequent to the validation of LINC01767 expression in HCC fresh frozen tissues through quantitative real time polymerase chain reaction, next generation sequencing was performed following LINC01767 over expression (GSE243371), and Gene Ontology/Kyoto Encyclopedia of Genes and Genomes/Gene Set Enrichment Analysis/ingenuity pathway analysis was carried out. In vitro experiment in Huh7 cell was carried out., Results: LINC01767 was down-regulated in HCC with a log fold change = 1.575 and was positively correlated with the cancer stemness. LINC01767 was a good diagnostic marker with area under the curve (AUC) [0.801, 95% confidence interval (CI): 0.751-0.852, P = 0.0106] and an independent predictor for overall survival (OS) with hazard ratio = 1.899 (95%CI: 1.01-3.58, P = 0.048). LINC01767 nomogram model showed a satisfied performance. The top-ranked regulatory network analysis of LINC01767 showed the regulation of genes participating various pathways. LASSO regression identified the 9-genes model showing a more satisfied performance than 5-genes model to predict the OS with AUC > 0.75. LINC01767 was down-expressed obviously in tumor than para-tumor tissues in our cohort as well as in cancer cell line; the over expression of LINC01767 inhibit cell proliferation and clone formation of Huh7 in vitro ., Conclusion: LINC01767 was an important tumor suppressor gene in HCC with good diagnostic and prognostic performance., Competing Interests: Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

There is an increased public concern about potential health hazards of exposure to electromagnetic radiation (EMR). To declare the carcinogenic effects of 1800 MHz EMR. In this study, Balb/c-3T3 cells were exposed to 1800 MHz EMR for 80 days. The cells were harvested for cell proliferation detection, cell cycle assay, plate clone, and soft agar formation assay, transwell assay, and mRNA microarray detection. 1800 MHz EMR promoted Balb/c-3T3 proliferation. No clones were observed in both plate clone and soft agar clone formation assay. The percentage of cells in S phase in Balb/c-3T3 cells of 80d Expo was obviously higher than the percetage in 80d Sham cells. 80d Expo Balb/c-3T3 cells had stronger migration ability than Sham cells. The mRNA microarray results indicated that cell cycle, cell division, and DNA replication were the main biological processes the significant genes enriched, with higher expression of RPs and Mcms. 1800 MHz EMR promoted Balb/c-3T3 cells proliferation and migration. The mRNA microarray results indicated that cell cycle, cell division, and DNA replication were the main biological processes the significant genes enriched. [ABSTRACT FROM AUTHOR]

Gliomas are the most commonly occurring primary malignant brain tumors in the central nervous system of adults. They are rarely curable and the prognosis for high grade gliomas is generally poor. Recently, long non‐coding RNA (lncRNA) human ovarian cancer‐specific transcript 2 (HOST2) has been reported to be expressed at high levels in human ovarian cancer, involving tumorigenesis. However, little is still known about whether and how HOST2 regulates glioma development and progression. Therefore, this study aims to investigate the role of HOST2 in human glioma cells. Reverse transcription quantitative real‐time polymerase chain reaction (RT‐qPCR) was used to determine the expression of lncRNA HOST2, let‐7b, and PBX3 in human glioma cells. Cultured human glioma cells were treated with siRNA (si)‐lncRNA HOST2, let‐7b mimic, si‐lncRNA HOST2 + let‐7b inhibitor, and si‐PBX3. Parameters including cell viability, colony formation, cell migration, and cell invasion were detected by cell counting kit‐8 assay, colony formation assay, scratch test, and Transwell assay respectively to determine the effects of down‐regulated HOST2 on glioma cells. Tumor formation in nude mice was evaluated by subcutaneous tumor formation experiment. Results showed that HOST2 and PBX3 were highly expressed in glioma tissue whereas let‐7b was expressed at much lower levels. In response to treatment with si‐lncRNA HOST2, si‐PBX3, and let‐7b mimic, glioma cell lines exhibited decreased cell viability, suppressed cell migration, invasion, and reduced colony formation of glioma cells. This was accompanied by an attenuated tumor formation with smaller volume and weight in nude mice, suggesting that down‐regulated HOST2 could inhibit the tumorigenicity of glioma cells. Lastly, we found that lncRNA HOST2 was highly expressed in glioma tissues and its down‐regulation could inhibit the growth and invasion of glioma cells. © 2018 IUBMB Life, 71(1):93–104, 2019 [ABSTRACT FROM AUTHOR]

Highlights • High positive rate of EBV in NPC tissues. • miR-BART4 highly expressed in EBV positive NPC tissues. • Inhibition of miR-BART4 suppresses growth and invasion and induces apoptosis of NPC. • EBVmay inhibit its radiosensitivity by overexpression of miR-BART4. • Overexpression of miR-BART4 regulates biological characteristics of NPC cells by targeting PTEN. Abstract Objective This study aims to explore the role of Epstein-Barr virus (EBV) miR-BART4 in occurrence and progression of nasopharyngeal carcinoma (NPC) and its effect on radiosensitivity. Method The expressions of EBV and miR-BART4 in 108 cases of NPC tissues and 97 cases of chronic nasopharyngeal inflammation tissues were determined by real time quantitative polymerase chain reaction (PCR), and the relationship between the expression of miR-BART4 and the clinicopathological features of NPC was analyzed. Cell lines, HONEl, CNEl, CNE2, C666-1, 6-10B, and NP-69 were used to compare the expression of miR-BART4, in which the CNE2 cells were selected for further experiments. CNE2 cells were grouped into blank group, negative control (NC) group, miR-BART4 inhibitors group and miR-BART4 mimics group. Cells in above groups were under radiation of 6 Gy X ray for 12 h before grouped into control group, 6 Gy group, NC + 6 Gy group, miR-BART4 inhibitors + 6 Gy group and miR-BART4 mimics + 6 Gy group. Cell proliferation, clone formation ability, cell apoptosis, invasion and migration ability were measured by MTT assay, clone formation assay, flow cytometry (FCM), Transwell assay and scratch test, respectively. Western blot analysis was used to detect the expression of apoptosis-related proteins (cleaved caspase-3, Bax and Bcl-2) and epithelial-mesenchymal transition (EMT) marker protein E-cadherin and Vimentin. mRNA and protein expression of PTEN were detected by qRT-PCR and western blot. Bioinformatics software and luciferase activity experiments were used to verify the targeting relationship between miR-BART4 and PTEN. Results Positive rate of EBV in NPC tissues (93.5%) was remarkably higher than that in chronic nasopharyngeal inflammation tissues (21.6%). miR-BART4 was highly expressed and mRNA and protein expression of PTEN was lowly expressed in EBV positive NPC tissues compared with EBV negative NPC tissues and chronic nasopharyngeal inflammation tissues. The expression of miR-BART4 was related to the clinical stage, lymph node metastasis and differentiation degree of NPC. Expression of miR-BART4 in CNE2, CNEl, HONEl, C666-1, 6-10B, 5-8F cells was higher than that in NP-69 cells. In CNE2 and C666-1 cell experiments, compared with blank group and NC group, miR-BART4 inhibitors group had decreased miR-BART4 expression, increased mRNA and protein expression of PTEN, cell survival rate, invasion and migration ability and increased cell apoptosis rate, which is totally contrary to the observation in miR-BART4 mimics group. The radiosensitive NPC tissues had higher miR-BART4 expression than that in radio-resistance NPC tissues. In comparison to 6 Gy group and NC + 6 Gy group, cell survival rate and clone number was inhibited, but the cell apoptosis rate was increased in miR-BART4 inhibitors +6 G group, in contrary to the observation in miR-BART4 inhibitors + 6 Gy group. Bioinformatics software and luciferase activity experiments confirmed that miR-BART4 could inhibit the expression of PTEN. Conclusion EBV may promote development and progression of NPC by up-regulating miR-BART4 expressions, consequently inhibiting its radiosensitivity, whose effect may be related to the targeting inhibition of PTEN expression. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Ovarian cancer is the most common malignant tumor in female reproductive system. Metformin is an orally taken hypoglycemic agent, which is extensively applied in the clinic. Clinical trials find that there may be a certain degree of action of the metformin in inhibiting malignant tumors. This paper aims to investigate the inhibitory effect and mechanism of metformin on human ovarian cancer cells. MATERIALS AND METHODS: Through in vitro cell experiment, the influences of metformin on the proliferation, colony formation and apoptosis of ovarian carcinoma cells were studied. Ovarian cancer cells SKOV-3 and A2780 in logarithmic growth phase were selected and cell proliferation was measured by MTT method. The metformin was processed for 48 h to calculate the survival rate of cells. Also, metformin was processed for 24 h and two weeks or stained with crystal violet, after which Quantity One (Bio-Rad, Hercules, CA, USA) method was used to quantitatively analyze the cell clone formation, meanwhile, the FCM (flow cytometry) was used for the detection and analysis. RESULTS: Intervened by metformin with different concentrations for 48 h, the cell viabilities of SKOV-3 and A2780 cells were respectively reduced by 19.49 ± 2.92%, 45.41 ± 7.95%, 53.84 ± 5.53%, 64.04 ± 4.36% and 11.45 ± 3.12%, 35.42 ± 7.55%, 43.77 ± 5.77%, 53.05 ± 5.55% as compared with that in the control group with statistical significances. After processed by metformin with different concentrations for two weeks, the cells clone numbers of SKOV-3 and A2780 were significantly reduced. Treatment of metformin on SKOV-3 and A2780 cells of human ovarian cancer showed significant apoptosis. CONCLUSIONS: The metformin has the inhibitory effect on the cells of human ovarian cancer, which may be through inducing ovarian cancer cell apoptosis. [ABSTRACT FROM AUTHOR]

The purpose of the research was aimed to explore the inhibition effect of 3,5,4'-trimethoxy-trans-stilbene (BTM) on human gastric cancer cells and its mechanism. The results indicated the higher the concentration of trimethoxystilbene was, the higher the inhibition rates on MKN-45 and MGC-803 cell lines were, with a significant dose-depending relationship. The half maximum inhibitory concentration of cisplatin on MKN-45 and MGC-803 cell lines treated with 20 μmol/l trimethoxystilbene were significantly lower than that of the control group (0 mol/l), showing that the cisplatin IC50 of MGC-803 cell lines could be reduced by trimethoxystilbene. In addition, the combination of trimethoxystilbene and cisplatin can obviously induce apoptosis of MKN-45 and MGC-803 cells, which is much higher than that of the single use of the two. The higher the concentration of trimethoxystilbene was, the higher the apoptosis rates of MKN-45 and MGC-803 cells were, there was a significant dose-effect relationship. And with the increased concentration of the drug, the proportion of G0/G1 was increased in a certain concentration effect relationship, suggesting that the G2/M phase of cisplatin resistant gastric cancer cell was blocked by trimethoxystilbene. Besides, trimethoxystilbene combined with cisplatin significantly inhibited the expression of anti-apoptotic protein Bcl-2, and increased the expression of Pro apoptotic protein Bax. [ABSTRACT FROM AUTHOR]

Background: Epithelial ovarian cancer (EOC) is the most common type of ovarian tumor, however, effective treatment does not currently exist for this condition. This study evaluated the role of vitexin in mitigating EOC both in vitro and in vivo ., Method: SKOV-3 cells were used for in vitro experimentation. Xenotransplantation mouse models were set up by subcutaneously injecting mice with SKOV-3 cells. CCK8 was used to screen the optimal dose in vitro . Cell proliferation, invasion, number of microtubule nodules and apoptosis were respectively detected by colony formation assay, transwell assay, microtubule formation assay and flow cytometry. TUNEL and immunohistochemistry were used to detect tissues apoptosis and VEGF content. Western blot assay was used to detect the expression of Ki67, caspase-3, VEGFA, VEGFR2, ERK1/2 and p38., Results: In vitro experiment, compared with the control group, 10 µL of vitexin significantly reduced Ki67 levels and enhanced tumor cell apoptosis rate. Additionally, the colony forming rate, invasive cells per field, and number of nodes/HPF in vitexin treated group decreased dramatically. The result of western blot showed that levels of p-p38/p38 and p-ERK1/2/ERK1/2 also noticeably decreased. In vivo experiment, 40 mg/kg of vitexin significantly inhibited tumor growth. In addition, vitexin significantly enhanced the percentage of tissues apoptosis, which was accompanied by a decrease in the percentage of VEGF-positive cells., Conclusions: Vitexin decreased the proliferation and invasion of SKOV-3 cells and noticeably reduced tumor growth. These findings suggest that vitexin could be a promising therapy for EOC., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at http://dx.doi.org/10.21037/atm-20-5586). The authors have no conflicts of interest to declare., (2020 Annals of Translational Medicine. All rights reserved.)

Our previous research confirmed the repression of SMADs signaling pathway inhibits the invasion, migration, and EMT in breast cancer MCF-7 and SKBR-3 cell lines by DNMT1 up-regulating CLDN6, but the mechanism is unclear. Western blot was performed to detect the expression of SMAD2, SMAD3, P-SMAD2, and P-SMAD3. Then RT-PCR was carried out to examine the expression of tight junctions and cell adhesion molecule E-cadherin. According to the gene sequence of Claudin6, shRNA was linked with the green fluorescent protein-expressing eukaryotic expression vector pGC silencer TMΜ6/Neo/GFP, and it was transfected into breast cancer MCF-7 cells and SKBR-3 cells. RT-PCR and western blot were applied to verify the Claudin6 gene-silencing effect. We observed cellular morphology with inverted microscope, analyzed the capacity for clone formation, and detected transepithelial electrical resistance. The level of MMP2, and MMP9 in the cells treated with or without SB431542 and MCF-7-shGFP, MCF-7-shClaudin-6, SKBR-3-shGFP, and SKBR-3-shClaudin-6 cells pretreated with SB431542 were examined by RT-PCR and western blot. The expressions of Claudin-6, occludin, and cell adhesion molecule E-cadherin were enhanced by SB431542. SB431542 transformed mesenchymal cell morphology into epithelial cell morphology, inhibited capacity for clone formation, increased transepithelial electrical resistance, and downregulated the expression of MMP2 and MMP9. Knock down of Claudin6 can abolish SB431542 effects. We conclude that Claudin6 mediates the effects of SB431542 on the biologic phenotypes of the breast cancer cells we studied. We speculate Claudin6-mediated the SB431542 inhibition of invasion, migration, and EMT in breast cancer cells via MMP2/9., Competing Interests: None., (IJCEP Copyright © 2020.)