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

Background 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). Methods 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. Results 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. Conclusion 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.