MALAT1 promotes proliferation, migration, and invasion of MG63 cells by upregulation of TGIF2 via negatively regulating miR-129.

Abstract

PurposeThis article aimed to investigate the mechanism by which MALAT1 and miR-129 affected the development of osteosarcoma.MethodsTumor tissues and adjacent tissues of 23 osteosarcoma patients were collected. Normal osteoblasts hFOB1.19 and osteosarcoma cells MG63 were cultured. MG63 cells were transfected and grouped: si-negative control (NC) group, si-MALAT1 group, miR-129 NC group, miR-129 mimics group, p-Empty vector group, p-MALAT1 group, p-MALAT1+ miR-129 mimics group, and p-MALAT1+ si-TGIF2 group. Luciferase reporter assay, Cell Counting Kit-8 assay, Transwell assay, quantitative reverse transcription PCR, Western blot, and Pearson correlation analysis were performed.ResultsMALAT1 expression in tumor tissues and MG63 cells was increased (P<0.01). High MALAT1 expression predicted poor prognosis of osteosarcoma patients. MG63 cells of si-MALAT1 group exhibited much lower cell viability, migration, and invasive cell numbers when compared with si-NC group (P<0.01). For MG63 cells of miR-129 mimics group, they had markedly lower cell viability, migration, and invasive cell numbers than miR-129 NC group (P<0.01). miR-129 was targetedly and negatively regulated by MALAT1. TGIF2, which was targetedly and negatively regulated by miR-129, was overexpressed in tumor tissues and MG63 cells (P<0.01). miR-129 overexpresison and TGIF2 downregulation significantly reversed the enhanced cell viability, migration, and invasion induced by MALAT1 (P<0.01).ConclusionMALAT1 promotes TGIF2 expression through negative regulation of miR-129, which further promotes the proliferation, migration, and invasion of MG63 cells.