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.
Highlights
Gastric cancer (GC) is the fifth most common cancer and the third-highest cause of death related to cancers worldwide [1, 2]
The results showed that the expression of matrix metalloproteinases 2 (MMP-2) and MMP-9 in AGS and HGC-27 cells was dramatically reduced by brain acid soluble protein 1 (BASP1) overexpression (P < 0:01) (Figure 4(c))
We demonstrated that BASP1 could suppress cell proliferation, migration, and invasion, as well as facilitate apoptosis through inhibiting the activation of the Wnt/β-catenin pathway in GC
Summary
Gastric cancer (GC) is the fifth most common cancer and the third-highest cause of death related to cancers worldwide [1, 2]. Over the past few decades, despite substantial improvements made in the treatment of GC patients, tumor recurrence and metastasis are still the leading causes of death in patients with GC [3, 4]. More and more studies have reported that BASP1 could regulate various types of cell biological behaviors including proliferation, apoptosis, and differentiation [6,7,8]. Increasing evidence has confirmed that BASP1, a potential tumor suppressor, plays an important role in a variety of cancers, such as thyroid cancer [5], liver cancer [9], and lung cancer [10]. The effect of BASP1 on GC has not yet been reported
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