| Background/Aim: Chronic inflammation has been hypothesized to play a significant role in the pathogenesis of gastric cancer. This study aimed to investigate the Hippo-YAP signaling pathway effects in the process of inflammation-induced gastric cancer.Methods: Human gastric epithelial cells were treated with MNNG or TNF-α to induce EMT, and levels of Hippo-YAP signaling pathway molecules were measured. At the same time, to observe the location of YAP molecule in GES-1 cells before and after the optimum stimulation conditions using immunofluorescence techniques.Transfection of YAP si RNA was used to silence Hippo-YAP signaling pathway to assess its involvement in this process. GES-1 cells were treated with MNNG in the same stimulation conditions,and determinate the content of the cell culture medium of TNF-α by ELISA. The relationship between Hippo-YAP signaling pathway and inflammation-induced gastric cancer was further analyzed in cells experiments.Results: MNNG- and TNF-α-induced gastric epithelial cells metaplasia and EMT were accompanied by YAP phosphorylation down-regulation and YAP nuclear translocation. Furthermore, knockdown of YAP gene reversed TNF-α-induced CDX2 up-regulation. MNNG treatment induced the expression of TNF-α in the GES-1 supernatants.Conclusion: TNF-α induced gastric epithelial cell metaplasia and EMT with suppressing Hippo-YAP signaling pathway, leading to YAP phosphorylation down-regulation and nuclear translocation. |
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