miR-23a suppresses pancreatic cancer cell progression by inhibiting PLK-1 expression

Abstract

The present study aimed to explore the effects and underlying mechanisms of microRNA (miR)-23a on pancreatic cancer (PC) cells progression. Reverse transcription-quantitative polymerase chain reaction and western blot analysis were used to detect the mRNA and protein miR-23a and PLK-1 level. Cell viability, cell cycle, migration and invasion assasy, and in vivo tumorigenicity assay were used to investigate the effects of miR-204. Further luciferase reporter assay was used to explore the mechanisms contributing to miR-204 effects. It was observed that miR-23a expression was upregulated and negatively associated with polo-like kinase-1 (PLK-1) expression in human PC tissues. PLK-1 was a direct target of miR-23a in PC cells. Functional analysis demonstrated that miR-23a overexpression suppressed cell proliferation, inhibited cell migration and invasion and promoted cell apoptosis in vitro. When PC cells were transfected with has-miR-23a PLK-1 was downregulated and its downstream molecules were deregulated, including decreased expression of B-cell lymphoma-2, cyclin B1 and vimentin, and increased expression of Bax and E-cadherin. The inhibitory effect of miR-23a on PC cell progression was observed in vivo tumor xenografts. The results of the study suggest that miR-23a inhibits PC cell progression by directly targeting PLK-1-associated signaling and promoting miR-23a expression may be a potential method for treating patients with PC.