BASP1 Suppresses Cell Growth and Metastasis through Inhibiting Wnt/<i>β</i>‐Catenin Pathway in Gastric Cancer
Li Li, Qinghua Meng, Guoying Li, Limei Zhao
Abstract
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 β ‐catenin in AGS and HGC‐27 cells were measured by western blot. In addition, the mRNA expressions of WT1, Wnt, and β ‐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 β ‐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/ β ‐catenin pathway in GC.