CeRNA network of lncRNA MIR210HG/miR-377-3p/LMX1A in malignant proliferation of glioma cells.

Abstract

Glioma represents the most heterogeneous and malignant form of brain tumor with a poor prognosis. The long non-coding RNA (LncRNA)-mediated competing endogenous RNA (ceRNA) network plays a regulatory role in cancer progression. The present study was conducted to expound on the role of lncRNA MIR210 host gene (MIR210HG)-mediated ceRNA mechanism in the malignant proliferation of glioma cells and provide a novel theoretical basis for the treatment of glioma. Expression levels of lncRNA MIR210HG, microRNA (miR)-377-3p, and LIM homeobox transcription factor 1 alpha (LMX1A) in glioma tissues and cells were determined by reverse-transcription quantitative polymerase chain reaction. Then, cell proliferation was assessed by cell counting kit-8 and colony formation assays. After that, the subcellular localization of lncRNA MIR210HG was analyzed by subcellular fractionation assay and the bindings of miR-377-3p to lncRNA MIR210HG and LMX1A were analyzed by the dual-luciferase assay. Glioma cells were transfected with si-MIR210HG, miR-377-3p inhibitor, or overexpressed-LMX1A vectors to evaluate their effects on the malignant proliferation of glioma cells. LncRNA MIR210HG was elevated in glioma tissues and cells and inhibition of lncRNA MIR210HG reduced the proliferation potential of glioma cells. LncRNA MIR210HG targeted and inhibited miR-377-3p and miR-377-3p targeted and inhibited LMX1A transcription. miR-377-3p downregulation or LMX1A overexpression reversed the inhibition of silencing lncRNA MIR210HG on glioma cell proliferation. LncRNA MIR210HG was upregulated in glioma tissues and cells and inhibition of lncRNA MIR210HG suppressed glioma cell proliferation through promoting miR-377-3p and repressing LMX1A.