Knockdown of PREX2a inhibits the malignant phenotype of glioma cells

Abstract

Glioma is the most common type of malignant brain tumor. Phosphatidylinositol‑3,4,5‑trisphosphate‑dependent Rac exchange factor 2a (PREX2a), which is a regulator of the small guanosine triphosphatase Rac, has previously been identified as an oncoprotein that inhibits phosphatase and tensin homolog deleted on chromosome 10 (PTEN) activity. However, the role of PREX2a in the regulation of the malignant phenotype of glioma has yet to be reported. The present study demonstrated that the mRNA and protein expression levels of PREX2a were significantly increased in glioma tissue, as compared with in normal brain tissue. Furthermore, the expression levels of PREX2a were positively correlated with tumor grade. PREX2a‑specific small interfering RNA‑mediated knockdown significantly inhibited proliferation and induced apoptosis of SWO‑38 glioma cells. Furthermore, inhibition of PREX2a expression significantly suppressed cell cycle progression in glioma cells, as detected by cell cycle arrest at G1 phase. In addition, knockdown of PREX2a inhibited the invasion of SWO‑38 glioma cells. The present study also investigated the molecular mechanisms underlying the effects of PREX2a knockdown, and demonstrated that phosphoinositide 3‑kinase signaling was significantly downregulated, which may be due to the upregulation of PTEN activity. In conclusion, the present study is the first, to the best of our knowledge, to suggest that knockdown of PREX2a may effectively inhibit the malignant phenotype of glioma in vitro; therefore, PREX2a may be considered a potential molecular target for the treatment of glioma.