LncRNA SNHG20 promotes tumorigenesis and cancer stemness in glioblastoma via activating PI3K/Akt/mTOR signaling pathway.

Long noncoding RNAs (lncRNAs) play crucial roles in the development of human cancers. LncRNA small nucleolar RNA host gene 20 (SNHG20) has been reported to be an oncogene in several cancers, whereas the specific role of SNHG20 in glioblastoma is unclear. In this study, we found that SNHG20 was significantly upregulated in glioblastoma tissues and cell lines. Survival analysis suggested that high expression of SNHG20 indicated the low overall survival rate of glioblastoma patients. Subsequently, gain or loss-of-function assays were carried out to examine the effect of SNHG20 on glioblastoma cell proliferation and apoptosis. We found that SNHG20 knockdown obviously suppressed cell proliferation, increased cell apoptosis and impaired stem properties, while SNHG20 overexpression led to the opposite results. In vivo experiment demonstrated that knockdown of SNHG20 efficiently suppressed cell growth in vivo. Furthermore, western blotting demonstrated that the PI3K/Akt/mTOR signaling pathway was activated by SNHG20 in glioblastoma cells. At last, rescue assays validated that PI3K/Akt/mTOR signaling pathway involved in the glioblastoma progression mediated by SNHG20. Taken together, this study revealed that SNHG20 regulated PI3K/Akt/mTOR signaling pathway to promote tumorigenesis and stemness of glioblastoma.