LncRNA MALAT1 promotes cell proliferation and invasion by regulating the miR-101/EZH2 axis in oral squamous cell carcinoma.

Abstract

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Emerging evidence indicates that long non-coding (lnc)RNAs play a key role in the cellular processes of tumor cells, including glycolysis, growth and movement. Here, the purpose of this study was to explore the biological functions and potential mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in OSCC. OSCC tissues and adjacent matched paraneoplastic normal tissues were collected from 20 OSCC patients. The expression of MALAT1 and miR-101 in OSCC tissues and cell lines (HSC3, SCC9, SCC15 and SCC25) were determined by real-time-polymerase chain reaction (qPCR). Caspase-3, xaspase-8 and EZH2 protein levels were determined by western blot analysis. MALAT1-mediated miRNAs were verified by bioinformatics analysis of StarBase and Luciferase reporter assay. Cell Counting Kit-8 (CCK-8) and Transwell assays were used for investigating MALAT1 effect on cell proliferation and invasion in the OSCC cells. qPCR analysis indicated that MALAT1 expression was obviously increased, and miR-101 was decreased in the OSCC tissues and cell lines. Functional studies revealed that overexpression of MALAT1 promoted OSCC cell proliferation and invasion. Further experiments revealed that miR-101 was a target of MALAT1 and that the miR-101 inhibitor abolished the effect of MALAT1 on OSCC cell proliferation and invasion. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) acted as a downstream effecter of MALAT1 in the OSCC cells. Collectively, these findings revealed that upregulation of MALAT1 facilitated OSCC proliferation and invasion by targeting the miR-101/EZH2 axis.