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.

多形性胶质母细胞瘤（GBM）是公认的最具侵袭性的脑肿瘤，预后差，1年和5年生存率低。GBM 的治疗方法有限且效率低下，迫切需要新的 GBM 治疗策略。MiR-338-3p被描述为多种恶性肿瘤（包括 GBM）的肿瘤抑制因子。然而，它在 GBM 中的作用尚不完全清楚。细胞或组织中靶标的 mRNA 或蛋白质水平分别通过定量逆转录 PCR (RT-qPCR) 或蛋白质印迹确定。GBM 细胞体外或体内的生长速率分别通过 Cell Counting Kit-8 或生物发光成像测量。hsa-miR-338-3p 的上调和磷脂酰肌醇 3,4,5-三磷酸依赖性 Rac 交换蛋白 2 蛋白的下调（与正常脑组织相比，在 GBM 组织中观察到Prex2 )。我们进一步证实鼠Prex2是 GBM 中 mmu-miR-338-3p 的靶标。Mmu-miR-338-3p 通过靶向Prex2在体外或体内对 GBM 细胞的生长产生深远的抑制作用，导致（蛋白激酶 B）AKT/信号转导和转录激活因子 3 (STAT3) 信号激活的减弱。mmu-miR-338-3p 的恢复或 Prex2 的抑制可能会促进 GBM 治疗创新疗法的发展。