The LncRNA MIAT is identified as a regulator of stemness-associated transcript in glioma.

BACKGROUND

Myocardial infarction-associated transcript (MIAT) is a long non-coding RNA (lncRNA) with altered expression in different diseases and malignancies. In this study, the potential expression and function of lncRNA MIAT in intuition and progression of brain cancer was investigated.

METHODS AND RESULTS

At first, TCGA data analysis demonstrated that lncRNA MIAT is significantly upregulated in various malignancies, especially its expression is dramatically elevated in brain tumors. In line with the data, we further evaluated the expression of MIAT in a series of brain tumor tissue, and our results revealed that the expression of MIAT was noticeably overexpressed in glioblastoma (p = < 0.0001). We further found that the expression of MIAT was markedly upregulated in low-grade brain tumors rather than high-grade ones. To further investigate the biological function of MIAT in brain cancer cells, its expression was suppressed by si-RNA-mediated knocking down. Inhibition of MIAT resulted in reduced proliferation of brain tumor cells followed by cell cycle arrest at the G1 phase, and significant induction of apoptosis, and senescence, but limited the migration ability and epithelial-mesenchymal-transition (EMT). Moreover, knocking-down of MIAT reduced the expression of stemness factors, followed by upregulation of their downstream miRNAs (micro RNAs), let-7a-5p, and miR-29b-3p.

CONCLUSIONS

Altogether, our data demonstrated that lncRNA MIAT could control proliferation, migration, and metastasis of brain cancer cells via regulating the Nanog/ Sox2 / let-7a-5p / miR-29b-3p axis. This data could introduce lncRNA MIAT as a novel oncogene in brain cancer pathogenesis.