STIM1 Deficiency In Intestinal Epithelium Attenuates Colonic Inflammation and Tumorigenesis by Reducing ER Stress of Goblet Cells
Xiaojing Liang, Jiansheng Xie, Hao Liu, Rongjie Zhao, Wei Zhang, Haidong Wang, Hongming Pan, Yubin Zhou, Weidong Han
Abstract
BACKGROUND & AIMS: entry, stromal interaction molecule 1 (STIM1) is known to promote colorectal cancer and T-cell-mediated inflammatory diseases. However, whether the intestinal mucosal STIM1 is involved in inflammatory bowel diseases (IBDs) is unclear. This study aimed to investigate the role of intestinal epithelial STIM1 in IBD. METHODS: ) were generated and induced to develop colitis and colitis-associated colorectal cancer. The mucosal barrier, including the epithelial barrier and mucus barrier, was analyzed. The mechanisms by which STIM1 regulate goblet cell endoplasmic reticulum stress and apoptosis were assessed. RESULTS: mice slightly shifted to an advantageous bacteria, which further protected the intestinal epithelium. CONCLUSIONS: Our results establish STIM1 as a crucial regulator for the maintenance of the intestinal barrier during colitis and provide a potential target for IBD treatment.