BASP1 Suppresses Cell Growth and Metastasis through Inhibiting Wnt/β-Catenin Pathway in Gastric Cancer

Objective. Our research is designed to explore the function of brain acid soluble protein 1 (BASP1) in the progression of gastric cancer (GC) and its underlying molecular mechanisms. Methods. In this study, the expression of BASP1 was detected by quantitative real-time polymerase chain reaction (qRT-PCR) in both GC tissue and GC cells. The cell cloning, proliferation, apoptosis, migration, and invasion potential of AGS and HGC-27 cells were, respectively, determined using colony formation assay, 5-ethynyl-20-deoxyuridine (EDU) assay, flow cytometry, and Transwell assay. The protein expressions of Bax, caspase-3, Bcl-2, matrix metalloproteinases 2 (MMP-2), MMP-9, Wilms tumor 1 (WT1), Wnt, and beta-catenin in AGS and HGC-27 cells were measured by western blot. In addition, the mRNA expressions of WT1, Wnt, and beta-catenin in AGS and HGC-27 cells were detected by qRT-PCR. Results. BASP1 expression was significantly downregulated in both GC tissue and GC cells. BASP1 overexpression markedly repressed proliferation, migration, and invasion and facilitated apoptosis in AGS and HGC-27 cells. In addition, BASP1 overexpression notably promoted the protein expression of Bax and caspase-3 in AGS and HGC-27 cells and inhibited the expression of Bcl-2, MMP-2, and MMP-9. Moreover, BASP1 overexpression significantly inhibited the mRNA and protein expression of WT1, Wnt, and beta-catenin in AGS and HGC-27 cells. Conclusion. BASP1 could significantly suppress cell proliferation, migration, and invasion and promote apoptosis through inhibiting the activation of the Wnt/beta-catenin pathway in GC.