MiR-495and MiR-551a Inhibit The Migration And Invasion Of Human Gastric Cancer Cells By Directly Interacting With PRL-3

Objective The main objective of the present study was to predict and identifymicroRNAs (miRNAs) that regulate peritoneal metastasis-associated molecule PRL-3in human gastric cancer (GC).Methods Four bioinformatics algorithms, and information from the existingliterature were combined to predict miRNAs binding to PRL-3. The expression ofcandidate miRNAs in cell lines and tissues was detected by real-time reversetranscriptase quantitative (qRT-PCR). miR-551a and miR-495, which considered asbinding to PRL-3were significantly down-expression in gastric cancer cell lines andgastric tissues. The mimics of miR-551a and miR-495were transfected into SGC7901and MKN28gastric cancer cell lines by Lipofectamine2000TMrespectively, cellswere also transfected with negative mimics as negative control. At24h aftertransfection, the expression of PRL-3mRNA in cells was detected by qRT-PCR, andthe PRL-3protein was analyzed by western blot. Finally, the invasion and migrationof gastric cancer cell lines after transfection were detected by transwell analysis.Results After gastric cancer cells transfected with miR-551a or miR-495mimics,both mRNA and protein levels of PRL-3were significantly reduced. Furthermore, themigration and invasion of GC cells were significantly inhibited by transfection withmiR-495or-551a mimics, indicating that PRL-3was a target of hsa-miR-551a andhsa-miR-495.Conclusion We propose that the effects of hsa-miR-551a and hsa-miR-495maybe, at least in part, caused by its regulation of PRL-3. Thus, a novel mechanism forthe regulation of PRL-3expression in gastric cancer cell has been identified. miRNAsmay be an attractive target for therapeutic intervention in advanced gastric cancer.