Lei Chen1, Xin Gong1, Mengyi Huang1. 1. Department of Neurosurgery, Hunan Provincial People's Hospital, (The First Affiliated Hospital of Hunan Normal University), Changsha, China.
Abstract
Background: 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. Objective: 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. Methods: 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. Results: 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. Conclusion: 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.
Background: 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. Objective: 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. Methods: 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. Results: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. Conclusion: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.