Overexpression of miR-31-5p inhibits human chordoma cells proliferation and invasion by targeting the oncogene c-Met through suppression of AKT/PI3K signaling pathway.

: Altered microRNA (miRNAs) expression has been reported in chordoma which has been considered as an important and complex disease. The study aims to explore the mechanism of miR-31-5p in chordoma in vitro. We firstly verified miR-31-5p level after mimics transfection using real-time PCR and found over-expressed miR-31-5p could inhibit cell growth and invasive ability, while induce cell apoptosis in vitro as detected by CCK8 assay, flow cytometry assay and transwell assay, respectively. Based on prediction result in silico, we validated the target gene C-met using dual-luciferase assay and detected the alternation of miR-31-5p as evidence. Using recombinant plasmid, we also found over-expressed c-Met could reduce the effect of over-expressed miR-31-5p on cell growth, cell cycle change, cell apoptosis and invasive ability as detected by CCK8 assay, flow cytometry assay and transwell assay respectively. Meanwhile, it was also appeared that the PI3K/AKT signaling pathway relevant proteins had alternation through WB assays in U-CH1 cells with treatment of miR-31-5p and c-met recombinant plasmid. miR-31-5p may play a protective role in chordoma patients by targeting c-met and then activating PI3K/AKT signaling pathway which suggested that alterations of miR-31-5p might be a useful biomarker and a potential therapy for early detection of chordoma as disease-related molecular and genetic changes.