Knockdown of Ras-Related Protein 25 (Rab25) Inhibits the In Vitro Cytotoxicity and In Vivo Antitumor Activity of Human Glioblastoma Multiforme Cells

• Published in: Oncology research 2017-03, Vol.25 (3), p.331-340
• Main Authors: Ding, Bingqian, Cui, Bei, Gao, Ming, Li, Zhenjiang, Xu, Chenyang, Fan, Shaokang, He, Weiya
• Format: Article
• Language: English
• Subjects: Animals; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Gene Expression Regulation, Neoplastic - genetics; Glioblastoma - genetics; Glioblastoma - pathology; Glioblastoma Multiforme (gbm); Humans; Invasion; Mice; Mice, Nude; Migration; Neoplasm Invasiveness - genetics; Phosphatidylinositol 3-Kinases - genetics; Phosphorylation - genetics; Proto-Oncogene Proteins c-akt - genetics; rab GTP-Binding Proteins - genetics; Ras-Related Protein 25 (rab25)
• ISSN: 0965-0407; 1555-3906
• DOI: 10.3727/096504016X14736286083065

Ras-related protein 25 (Rab25) is a member of the Rab family, and it has been reported to play an important role in tumorigenesis. However, its direct involvement in human glioblastoma multiforme (GBM) is still unclear. The aim of the current study was to investigate the potential role of Rab25 in the growth, proliferation, invasion, and migration of human GBM. Our results showed that Rab25 expression was significantly higher in human GBM cell lines compared with a normal astrocyte cell line. In vitro functional studies revealed that knockdown of Rab25 reduced cell proliferation and inhibited invasion and migration of GBM cells. In vivo experiments showed that knockdown of Rab25 attenuated the tumor growth in nude mice. Finally, knockdown of Rab25 significantly inhibited the phosphorylation levels of PI3K and AKT in GBM cells. Taken together, these findings indicate that Rab25 may act as a tumor promoter in human GBM and that approaches to target Rab25 may provide a novel strategy to treat this disease.