RAB43 Promotes Gastric Cancer Cell Proliferation and Metastasis via Regulating the PI3K/AKT Signaling Pathway

Background: Ras-related GTP-binding protein 43 (RAB43) plays a key part in the progression of many human cancers. However, the role and functional mechanisms of RAB43 in gastric cancer (GC) remain unknown. Purpose: To elucidate the function and mechanism of RAB43 in the progression of GC. Patients and Methods: One hundred patients with histologically confirmed GC were recruited for this study. Tumor samples and GC cell lines were used to detect RAB43 levels. Cell Counting Kit8 (CCK8) and colony formation assays were used to analyze cell proliferation. Cell migration and invasion ability were examined by wound healing and transwell assays. Western blot assays and quantitative real-time PCR (qRT-PCR) were performed to examine related mRNA and protein expression. In vivo experiments were used to examine the effect of RAB43. Results: Patients with RAB43-positive tumors had worse overall survival than patients with RAB43-negative tumors. Downregulation of RAB43 significantly inhibited cell proliferation and cell metastasis. In contrast, RAB43 overexpression promoted proliferation and metastasis in normal gastric epithelial GES-1 cells. In vivo studies confirmed that RAB43 promoted tumor growth. In addition, the knockdown of RAB43 significantly inhibited cell proliferation and metastasis via phosphatidylinositol-3-kinases/protein-serine-threonine kinase (PI3K/AKT) pathway. Conclusion: RAB43 promotes GC cells proliferation and migration in vivo and in vitro and probably served as a novel potential therapeutic biomarker for GC.