LncRNA SOX2-OT regulates miR-192-5p/RAB2A axis and ERK pathway to promote glioblastoma cell growth

基因敲除 生物 SOX2 MAPK/ERK通路 细胞生长 癌症研究 信号转导 细胞生物学 分子生物学 细胞培养 转录因子 基因 遗传学
作者
Hongcai Wang,Qinglei Hu,Yi-Lei Tong,Shiwei Li,Maosong Chen,Boding Wang,Haimeng Li
出处
期刊:Cell Cycle [Taylor & Francis]
卷期号:20 (19): 2010-2020 被引量:14
标识
DOI:10.1080/15384101.2021.1965722
摘要

Glioblastoma (GBM) is the most frequent tumor in the central nervous system. Long non-coding RNAs (lncRNAs) have been widely accepted as essential participators in cancer progression. Nonetheless, the specific role and mechanism of lncRNA SRY-box transcription factor 2 overlapping transcript (SOX2-OT) in GBM have not been studied. We evaluated expression levels of SOX2-OT, miR-192-5p and Ras-related protein Rab-2A (RAB2A) in GBM cells via qRT-PCR. To investigate the roles of SOX2-OT in GBM cells, CCK-8, JC-1, EdU, and western blot assays were performed. The connection among SOX2-OT, miR-192-5p and RAB2A in GBM cells was explored through pull down, luciferase reporter, and RIP assays. Western blot and qRT-PCR were employed to analyze the activity of extracellular-signal-regulated kinase (ERK) signaling pathway. SOX2-OT expression was higher in GBM cell lines than in normal cells. SOX2-OT knockdown repressed proliferation and promoted apoptosis of GBM cells. Mechanism assays revealed that SOX2-OT could sponge miR-192-5p. Moreover, RAB2A was certified to be the target gene of miR-192-5p. Overexpression of RAB2A reversed the repressive function of SOX2-OT knockdown on GBM cell growth. Furthermore, SOX2-OT activated ERK signaling pathway in GBM cells. SOX2-OT regulated miR-192-5p/RAB2A axis and ERK pathway to promote GBM cell growth.

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