Abstract
Glioma is one of the most malignancy and prevalent tumor in the human central nervous system, which is associated with severe morbidity and high mortality. Numerous studies have explained the clear correlation between abnormal expression of lncRNA and progression of Glioma. LncRNA small nucleolar RNA host gene 4 (SNHG4) have been proved to play oncogenesis roles in various tumors, however, the underlying mechanism remains to be explored deeply. In this study, by analysis of the public database, we found that SNHG4 was upregulated in multiple cancer tissues, including glioma. Subsequently, the functional roles of SNHG4 were investigated, and we found that knockdown of SNHG4 remarkedly inhibited cell proliferation, migration. While, overexpression of SNHG4 enhanced these functions of glioma cells in vitro. Meanwhile, as the in vivo tool, zebrafish xenograft model was used to verify the functions of SNHG4 in glioma cells. Mechanically, we identified that SNHG4 or MYO1B could bind with miR-367-3p by the luciferase reporter assays. Furthermore, the rescue experiments showed that the inhibition of miR-367-3p or the expression of MYO1B partially rescue the inhibition effects of SNHG4 in glioma cells. Our study reveals that SNHG4 promotes the proliferation, migration of glioma via regulating miR-367-3p/MYO1B axis.