Abstract

Objective To investigate the regulatory effect of transforming growth factor-β1 (TGF-β1) via Wnt signaling pathway in gastric cancer cells. Methods Via 5, 10, 20 ng/ml TGF-β1 recombinant protein inducing or TGF-β1 small interfering RNA (siRNA) recombinant plasmid gene silencing in gastric cancer cell MGC803, detect the expression of protein related to the occurrence and progression of gastric cancer by Western blotting. Results In gastric cancer cells, TGF-β1 can induce high expression of Wnt3a, β-catenin and Cyclin D1 , while their expression increase with increased TGF-β1 recombinant protein concentration (Wnt3a control group: 1.000±0.046; 5ng/ml group: 1.233±0.033, P=0.025; 10 ng/ml group: 2.233±0.122, P=0.001; 20 ng/ml group: 3.200±0.151, P=0.000. β-catenincontrol group: 1.000±0.035; 5 ng/ml group: 1.867±0.120, P=0.003; 10 ng/ml group: 2.200±0.153, P=0.002; 20 ng/ml group: 1.967±0.120, P=0.002. Cyclin D1control group: 1.000±0.029; 5 ng/ml group: 1.100±0.100, P=0.435; 10 ng/ml group: 3.167±0.176, P=0.000; 20 ng/ml group: 2.867±0.203, P=0.001). And silencing TGF-β1gene leads to low expression of Wnt3a, β-cateninand Cyclin D1 (Wnt3a control group: 1.000±0.040; siRNA group: 0.400±0.058, P=0.002. β-catenin NC: 1.000±0.046; siRNA group: 0.467±0.033, P=0.001. Cyclin D1 control group: 1.000±0.029; siRNA group: 0.333±0.088, P=0.003). Conclusion TGF-β1 plays a positive role in the Wnt3a/β-catenin signaling pathway in gastric cancer cells, and can regulate the epithelial-mesenchymal transition (EMT) process of gastric cancer cells by activating Wnt3a/β-catenin signaling pathway. Key words: Gastric cancer; Transforming growth factor-β1; Wnt signaling pathway

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