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High miR-3609 expression is associated with better prognosis in TNBC based on mining using systematic integrated
Rumeng Ding1, Zhenfeng Duan1,2, Meng Yang1
1Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Abstract:
MicroRNAs (miRNAs/miRs) are small endogenous RNAs that regulate gene expression post-transcriptionally. Abnormal miR-3609 expression is associated with the occurrence of pancreatic cancer, glioma and other diseases, such as polycystic ovary syndrome. However, the prognostic potential of miR-3609 has been reported in breast cancer. Thus, the present study aimed to investigate the differential expression and prognostic value of miR-3609 in patients with breast cancer from the UALCAN, cBioportal and Kaplan-Meier Plotter databases, respectively. Furthermore, the co-expression genes of miR-3609 in breast cancer were investigated using data from the LinkedOmics database, and functional enrichment analysis was performed using the LinkInterpreter module in LinkedOmics. The co-expression gene network was constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins database, and the cytoHubba plug-in was used to identify the hub genes, which were visualized using Cytoscape software. The prognoses of the hub genes were performed using the Kaplan-Meier Plotter database. The Cell Counting Kit-8 and cell cycle assays were performed to confirm the functions of miR-3609 mimics transfection in MDA-MB-231 cells. Survival analysis using the Kaplan-Meier Plotter database demonstrated that high miR-3609 expression in triple-negative breast cancer (TNBC) was associated with a better prognosis. Furthermore, the experimental results indicated that high miR-3609 expression inhibited the proliferation of TNBC cells and induced cell cycle arrest of TNBC cells in the G0/G1 phase. Taken together, the results of the present study suggest that miR-3609 plays a vital role in mediating cell cycle arrest and inhibiting the proliferation of TNBC cells.
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