YY1-Activated Long Noncoding RNA SNHG5 Promotes Glioblastoma Cell Proliferation Through p38/MAPK Signaling Pathway

Glioma is considered one of the most prevalent and lethal brain tumors. Glioblastoma (GBM) is a main subtype of glioma. Long non-coding RNAs (lncRNAs) are identified as a new class of biomarkers and therapeutic targets for treatment of GBM. In the present study, we focused on exploring the function and potential mechanistic regulation of lncRNA small nucleolar RNA host gene 5 (SNHG5) in GBM. Gene expression was determined by qRT-PCR or western blot, as appropriate. CCK-8 and EdU assays, flow cytometry analysis and caspase 3 activity assay were conducted to evaluate several cellular processes in GBM cells. The relationship between YY1 and SNHG5 was assessed via ChIP and luciferase reporter assays. SNHG5 was highly expressed in GBM. Loss- and gain-of-function assays revealed that SNHG5 promoted GBM cell proliferation and inhibited cell apoptosis in GBM. Mechanism experiments proved Yin Yang 1 (YY1) as transcriptional activator of SNHG5 in GBM. More importantly, we found that SNHG5 played the oncogenic role in GBM by activating p38/MAPK signaling pathway. YY1-induced SNHG5 promoted the cell proliferation in GBM via p38/MAPK signaling pathway. The findings expanded our understanding of SNHG5 as an oncogene in GBM.