RAB1A regulates glioma cellular proliferation and invasion via the mTOR signaling pathway and epithelial–mesenchymal transition

• Published in: Future oncology (London, England) Vol. 17; no. 24; pp. 3203 - 3216
• Main Authors: Ren, Bingcheng, Wang, Le, Nan, Yang, Liu, Tong, Zhao, Liwen, Ma, Haiwen, Li, Jiabo, Zhang, Yiming, Ren, Xiao
• Format: Journal Article
• Language: English
• Published: England Future Medicine Ltd 01.08.2021
• Subjects: Animals; Brain Neoplasms - pathology; brain slice; Cell Proliferation - physiology; Epithelial-Mesenchymal Transition - physiology; epithelial–mesenchymal transition; glioma; Glioma - pathology; Heterografts; Humans; invasion; Mice; Mice, Nude; mTOR; Neoplasm Invasiveness - pathology; proliferation; rab1 GTP-Binding Proteins - metabolism; RAB1A; RAC1; Signal Transduction - physiology; TOR Serine-Threonine Kinases - metabolism; RAB1A; epithelial–mesenchymal transition; brain slice; invasion; proliferation; mTOR; glioma; RAC1
• ISSN: 1479-6694; 1744-8301
• DOI: 10.2217/fon-2021-0116

We aimed at investigating the mechanism of RAB1A proliferation and invasion in gliomas. Genome-wide expression profile data and immunohistochemistry were analyzed to assess expression in gliomas. The Transwell assay, wound healing assay, brain slice coculture model, cellular fluorescence and intracranial xenograft model of nude mice were used to determine the proliferation and invasion of glioma cells. was highly expressed in gliomas compared with normal brain tissue. The overall survival time of glioma patients with high expression was significantly shortened. RAB1A regulated the activity of RAC1 by inhibiting the mTOR signaling pathway, affecting actin polymerization, cell morphology and cell polarity. downregulation inhibited the epithelial–mesenchymal transition, proliferation and invasion of glioma cells.