Phosphatidylinositol 3,4,5-Trisphosphate-Dependent Rac Exchanger 2 Protein Facilitates Glioma Progression via Akt and Stat3 Signaling.

Glioblastoma multiforme (GBM) is the recognized as the most aggressive brain tumor with poor prognosis and low 1-year and 5-year survival rate. The treatment methods for GBM are limited and inefficient, and novel strategies for GBM treatment are urgently warranted. MiR-338-3p is described as a tumor suppressor in a variety of malignancies, including GBM. However, its role in GBM is not fully understood. The mRNA or protein levels of targets in cells or tissues were determined by quantitative reverse transcription PCR (RT-qPCR) or Western blot, respectively. The GBM cell growth rate in vitro or in vivo was measured by Cell Counting Kit-8 or bioluminescence imaging, respectively. Upregulation of hsa-miR-338-3p and downregulation of phosphatidylinositol 3,4,5-trisphosphate-dependent Rac exchanger 2 protein (Prex2) were observed in GBM tissues compared to normal brain tissues. We further confirmed that murine Prex2 was a target of mmu-miR-338-3p in GBM. Mmu-miR-338-3p exerted profound inhibition effects on GBM cell growth in vitro or in vivo through targeting Prex2, leading to attenuation of (Protein kinase B) AKT/Signal transducer and activator of transcription 3 (STAT3) signaling activation. Restoration of mmu-miR-338-3p or inhibition of Prex2 may facilitate the development of innovative therapies for GBM treatment.