Long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been shown to play a critical role in the development of several malignancies. However, the potential molecular mechanism of MALAT1 in glioma remains unclear. In the present study, we found that the expression of MALAT1 was aberrantly increased in both human glioma tissues and cells and associated with poor prognosis in glioma patients. We further found that MALAT1 silencing significantly inhibited glioma cell proliferation while induced cell cycle arrest and apoptosis. In parallel, knockdown of MALAT1 decreased tumor volume in vivo. These results suggested that MALAT1 acts as a functional oncogene, resulting in the oncogenicity in glioma. Nevertheless, the tumor-suppressive effect of MALAT1 silencing was reversed by miR-124. Besides, the relevance of ZEB2 in tumor progression has been studied in several forms of human cancer, and ZEB2 was identified as a target of miR-124 and negatively regulated by miR-124. MALAT1 overexpression or miR-124 inhibitor led to increased expression of ZEB2. In summary, our study depicts a novel pathway of MALAT1/miR-124/ZEB2 that regulates the progression of glioma and might provide a promising strategy for glioma therapy.
Keywords: Glioma; LncRNA; MALAT1; ZEB2; miR-124.