MiR-206 inhibits proliferation and migration of prostate cancer cells by targeting CXCL11.

Abstract

Our study was aimed at detecting the expression levels of miR-206 in prostate cancer (PCa) tissues and PCa cell lines, and exploring the potential functions of miR-206 by targeting chemokine ligand 11 (CXCL11). RT-qPCR was applied to detect the expressions of miR-206 and CXCL11 in PCa tissues and in PCa cell lines. Expression of the CXCL11 protein was detected using Western blot. After manipulating the expression of miR-206 and CXCL11 in PC-3 and DU-145 cells, the changes of cell proliferation and cell cycle were observed through cell counting kit-8 (CCK-8) and flow cytometry. Wound healing and transwell assay were conducted for cell migration and invasion examination in vitro. The luciferase reporter assay was applied to validate the association between miR-206 and CXCL11. MiR-206 was significantly under-expressed in PCa tissues and in PCa cell lines. Up-regulation of miR-206 could inhibit proliferation, migration, invasion and induced G1/G0 arrest of PCa cells, and vice versa. MiR-206 bound to the 3'-UTR of CXCL11 and significantly repressed the luciferase activity. Overexpression of miR-206 decreased the expression level of CXCL11 significantly. CXCL11 mRNA and protein levels were significantly decreased in PCa cells. Downregulation of CXCL11 presented tumor-suppressing effects on PCa cells as miR-206 mimics did. And co-transfection miR-206 attenuated the tumor-promoting effects induced by CXCL11 overexpression. Our current finding demonstrated that miR-206 negatively regulated PCa cell proliferation and migration, and arrested cell cycle by targeting CXCL11 as a tumor suppressor in prostate cancer.