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The present study investigated the molecular mechanism by which microRNA-206 (miR-206) targets Annexin A2 (ANXA2) expression and inhibits the invasion and metastasis of prostatic cancer cells through regulation of the epithelial-mesenchymal transition (EMT). Using bioinformatics analysis, miR-206 was identified as the most promising candidate miRNA that targeted ANXA2 . Prostate tissue specimens from 60 patients with prostate cancer, 30 patients with metastatic prostate cancer and 20 patients with benign prostatic hyperplasia (BPH) were examined for ANXA2 protein expression by immunohistochemistry and western blotting and for miR-206 expression by reverse transcription-quantitative polymerase chain reaction. Additionally, human prostate cancer PC-3 cells were transfected with miR-206 mimics, miR-206 inhibitors or a negative control sequence, and expression of ANXA2, E-cadherin and N-cadherin was detected by western blotting. Transwell assays were performed to determine the effect of altered miR-206 expression on the invasive behavior of PC-3 cells. Bioinformatics analysis predicted complementary binding between miR-206 and ANXA2 mRNA. ANXA2 protein expression was detected in a significantly higher proportion of BPH tissues (95%, 19/20) when compared with prostate cancer tissues (51.7%, 31/60; P&lt;0.05). Similarly, ANXA2 was expressed in a significantly higher proportion of metastatic prostate cancer samples than that of prostate cancer samples (P&lt;0.05). Expression of miR-206 was higher than that of ANXA2 in prostate cancer samples, but lower in BPH samples. Inhibition of miR-206 expression in PC-3 cells upregulated ANXA2 and E-cadherin protein expression levels, downregulated N-cadherin and vimentin, and promoted cell invasion in vitro . These data suggested that binding between miRNA-206 and ANXA2 mRNA may regulate EMT signaling, thereby suppressing the invasion and metastasis of prostatic cancer cells.

MicroRNA‑206 regulates the epithelial‑mesenchymal transition and inhibits the invasion and metastasis of prostate cancer cells by targeting Annexin A2