Background: RAB3A-interacting protein (Rab3IP) is known to be involved in cancer; however, its function during the proliferation of gastric cancer (GC) cells remains unknown. Therefore, this study aimed to explore the potential function of Rab3IP in GC. Methods: The expression of Rab3IP and its clinical pathology value were determined by quantitative real-time PCR and immunohistochemistry. Rab3IP (knockdown and overexpression) and light chain 3 (LC3) lentiviruses were transfected into GC cells, and cell proliferation was measured using cell counting kit-8, plate clone formation, flow cytometry, and tumorigenesis assays. Cell autophagy was measured using a confocal laser scanning microscope and by western blotting. Luciferase reporter assay was performed to analyse the regulation of Rab3IP by microRNA-532-3p (miR-532-3p). Results: Overexpression of Rab3IP in GC samples enhanced the cell proliferation ability, but decreased the number of autophagosomes and expression of LC3-II and sequestosome-1 (SQSTM1 or p62) markers. Furthermore, we found that miR-532-3p can bind to the 3'UTR region of RAB3IP and inhibit the proliferation ability of GC cells. Further, the expression of miR-532-3p negatively correlated with that of Rab3IP. Conclusions: Our study elucidates the central role of Rab3IP in inducing proliferation of GC cells through its involvement in autophagy. miR-532-3p directly targets Rab3IP and represses its function, thereby demonstrating a novel regulatory link in GC.
Keywords: Rab3IP; cell autophagy; cell proliferation; gastric cancer; miR-532-3p.