IGHG1 induces EMT in gastric cancer cells by regulating TGF-β/SMAD3 signaling pathway

Objective: Gastric cancer is one of the most common malignant tumors in the world. IGHG1 is a differentially expressed protein screened out in gastric cancer in the early stage of the subject group. This topic explores the expression of IGHG1 in gastric cancer and the effect of IGHG1 on the proliferation, migration, invasion and EMT of gastric cancer SGC7901 cells and its mechanism of action. Methods: Twenty cases of gastric cancer were purified by laser Capture Microdissection. The isotopic tags for relative and absolute quantification was used to label the proteins, and then analyzed and identified them by quantitative proteomics. Immunohistochemical staining method was used to detect the expression of IGHG1 protein in gastric cancer tissues. Western blot was used to detect the expression of IGHG1 in gastric cancer cells. The MTT and Petri dish clone formation experiment analyzed the effect of low expression of IGHG1 on the proliferation of SGC7901 cells. Scratch test and Transwell migration and invasion test to observe the effect of low expression of IGHG1 on the migration and invasion of SGC7901 cells. Western blot was used to detect the effect of low expression of IGHG1 on the expression of EMT-related proteins. Results: 243 proteins related to gastric mucosal lesions were preliminarily identified. We found that IGHG1 is highly expressed in gastric cancer tissues compared with normal control tissues. IGHG1 promotes the proliferation, migration and invasion of gastric cancer cells. Compared with the control group, the expression of EMT-related proteins Vimentin, N-cadherin, TGF-β, P-SMAD3 was decreased and the expression of E-cadherin was increased after IGHG1 low expression. Conclusions: IGHG1 induces EMT in SGC7901 cells by regulating the TGF-β/SMAD3 signaling pathway.