ABSTRACT
@#[Abstract] Objective: To investigate the effect of miR-383-5p on the proliferation and invasion of medulloblastoma (MB) by targeting DNA mismatch repair MSH6 gene. Methods: A total of 15 pairs of tumor tissues and corresponding adjacent tissues from MB patients, who were surgically treated and pathologically confirmed in the Department of Oncology of the Second Affiliated Hospital of Hainan Medical College from July 2014 to May 2017, were collected for this study. qPCR was applied to detect the expression of miR-383-5p in MB tissues and cell lines. The experimental cells were divided into control group (NC group), miR-383-3p overexpression group (miR-383-5p group), MSH6 knockdown group (si-MSH6 group) and miR-383-5p inhibitor+si-MSH6 group. CCK-8 assay was used to detect the proliferation of UW473 cells. Transwell assay was used to examine the invasion and migration of UW473 cells, the targeting relationship between miR-383-5p and MSH6 was verified by Dual-luciferase reporter gene assay, and Western blotting (WB) was performed to detect the protein expression of MSH6. Results: The expression level of miR-383-5p was significantly down-regulated in MB tissues and cell lines compared with para-cancer tissues (all P<0.05 or P<0.01). Overexpression of miR-383-5p significantly inhibited the proliferation, migration and invasion of UW473 cells (all P<0.05 or P<0.01), and down-regulated the expression level of MSH6 (all P<0.01). Dual-luciferase reporter gene assay demonstrated that miR-383-5p could targetedly bind to the 3'UTR of MSH6. Knockdown of MSH6 could inhibit the proliferation, invasion and migration of UW473 cells (all P<0.01). Further experiments showed that simultaneous knockdown of miR-383-5p and MSH6 could attenuate the inhibition of MSH6 silence on the proliferation, invasion and migration of UW473 cells. Conclusion: miR-383-5p expression is down-regulated in MB tissues and cell lines, and miR-383-5p suppresses the proliferation, migration and invasion of UW473 cells via targetedly down-regulating MSH6.