Long non-coding RNA SNHG16 contributes to glioma malignancy by competitively binding miR-20a-5p with E2F1.

Glioma is among the most fatal and highly aggressive primary malignant tumors in the central nervous system. Small nucleolar RNA host gene 16 (SNHG16) is identified to play an oncogenic role in several cancers. However, the exact mechanism of SNHG16 action in the regulation of glioma development remains unknown. LncRNA SNHG16 was increased in glioma tissues and cells compared with normal brain tissues and cells. SNHG16 expression was correlated with the malignancy and poor prognosis of glioma patients. SNHG16 and E2F1 contained a binding site of miR-20a-5p. miR-20a-5p was decreased in glioma tissues and cells compared with normal brain tissues and cells. Downregulation of miR-20a-5p was correlated with the malignancy and poor prognosis of glioma patients. In glioma tissues, the expression of SNHG16 was negatively correlated with miR-20a-5p. Downregulation of SNHG16 increased miR-20a-5p expression. miR-20a-5p mimic reduced the luciferase activity of SNHG16 and E2F1; miR-20a-5p mimic enhanced the inhibition of cell proliferation, invasion, migration, and EMT, and increase of apoptosis induced by SNHG16 knockdown. Anti-miR-20a-5p reversed the effects of shSNHG16. We also found that SNHG16 may act as a ceRNA for miR-20a-5p, enhancing the expression of E2F1. Additionally, knockdown of SNHG16 remarkably reduced the increase of tumor volumes in xenograft mouse models. In tumor tissues, knockdown of SNHG16 increased the expression of miR-20a-5p, reduced EMT and increased apoptosis. In conclusion, SNHG16 promotes glioma tumorigenesis by sponging miR-20a-5p, leading to the enhancement of its endogenous targets E2F1. The data provides a new clue for the role of SNHG16/miR-20a-5p/E2F1 in the development of glioma.