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. 2017 Jun;13(6):3309-3314.
doi: 10.3892/etm.2017.4387. Epub 2017 Apr 26.

miRNA-186 inhibits prostate cancer cell proliferation and tumor growth by targeting YY1 and CDK6

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"VSports" miRNA-186 inhibits prostate cancer cell proliferation and tumor growth by targeting YY1 and CDK6

V体育2025版 - Shu Lu et al. Exp Ther Med. 2017 Jun.

Abstract (VSports手机版)

microRNAs (miRNAs) are known to be important in tumor initiation and progression VSports手机版. Recent studies have demonstrated that miR-186 is critical in several types of cancer, including human non-small cell lung cancer, bladder cancer and pancreatic ductal adenocarcinoma. However, the functions of miR-186 in prostate cancer (PCa) are still unclear. In the present study, downregulation of miR-186 in PCa cells was detected when compared with the normal prostate cell line. When miR-186 overexpressed in PCa cells, cell proliferation in vitro was evidently inhibited as shown using cell counting kit-8 assays and cell-cycle analysis, and tumor growth in vivo was decreased as shown by tumor growth assays in nude mice. Furthermore, through bioinformatics prediction and biochemical analyses, Yin Yang 1 (YY1) and cyclin-dependent kinase 6 (CDK6) have been proven to act as direct targets of miR-186. These results indicate that miR-186 is a negative regulator in PCa by inhibiting PCa cell proliferation via targeting YY1 and CDK6. .

Keywords: Yin Yang 1; cell proliferation; cyclin-dependent kinase 6; miR-186; microRNA; prostate cancer; tumor growth V体育安卓版. .

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"VSports最新版本" Figures

Figure 1.
Figure 1.
Expression levels of miR-186 in prostate cancer cell lines. The expression of miR-186 in adult human prostatic epithelial cells and human prostate cancer cell lines were analyzed using quantitative polymerase chain reaction. ***P<0.001 vs. RWPE-1. miRNA, microRNA.
Figure 2.
Figure 2.
miR-186 inhibits prostate cancer cell proliferation. (A) The miR-186 expression level in PC-3 cells after transfection with pCDH-miR-186 or pCDH were detected using quantitative polymerase chain reaction, where pCDH acted as a negative control. (B) The cell cycle phases of PC-3 cell transfection with pCDH-miR-186 or pCDH were analyzed using flow cytometry, where pCDH acted as a negative control. (C) Effect on cell proliferation of miR-186 overexpression in PC-3 cells was determined by the Cell Counting Kit-8 assay, where pCDH acted as a negative control. *P<0.05, **P<0.01 and ***P<0.001. miRNA, microRNA.
Figure 3.
Figure 3.
miR-186 suppresses tumor growth of prostate cancer cells in vivo. (A) Four weeks after PC-3/pCDH and PC-3/miR-186 cells were injected into the subcutaneous, mice were euthanized and examined for the growth of subcutaneous tumor. (B) Tumor sizes and (C) weights from the mice in the experiment were measured. ***P<0.001. miRNA, microRNA.
Figure 4.
Figure 4.
YY1 and CDK6 are direct targets of miR-186. (A) The mRNA levels of predicted target genes of miR-186 in PC-3/miR-186 and PC-3/pCDH cells were detected using quantitative polymerase chain reaction. (B) Effects of miR-186 overexpression on the activity of the 3′-UTRs of target genes in PC-3 cells were analyzed by the dual luciferase reporter assay, where PC-3/pCDH acted as a negative control. (C) Effects of miR-186 expression on the activity of wild-type and mutant 3′-UTRs of YY1 and CDK6 were analyzed by the dual luciferase reporter assay. (D) Effects of miR-186 overexpression in PC-3 cells on the expression of YY1 and CDK6 were detected by Western blotting, where PC-3/pCDH acted as negative controls. *P<0.05, **P<0.01 and ***P<0.001. N.S, no significance; YY1, Yin Yang 1; CDK6, cyclin-dependent kinase 6; UTRs, untranslated regions; miRNA, microRNA.

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