Abstract
MUC2 produced by goblet cells is the gel forming mucin in mucus that protects the intestinal epithelium against harmful substances and the development of tumors. In this study, we investigated the role of MUC2 in colonic epithelial cell apoptosis, a process essential in preventing tumor formation. A high MUC2‐producing colonic goblet cell line (HT29‐H) and a clone silenced for MUC2 (HT29‐L) by lentivirus‐shRNA were used. Cells were exposed to apoptosis‐inducing agents and apoptosis quantified by caspase 3 and Poly (ADP‐ribose) polymerase cleavage, DNA fragmentation and lactate dehydrogenase (LDH) release. Expression of endoplasmic reticulum (ER) stress markers was evaluated to monitor ER activities as well as expression of genes involved in MUC2 biosynthesis. HT29‐H was found to be highly susceptible to apoptosis as compared to HT29‐L cells. Over expression of MUC2 in HT29‐H cells caused increased expression of ER stress markers and decreased MUC2 folding genes as compared to HT29‐L or parental wild‐type cells. Our findings indicate that MUC2 induces apoptosis in an ER stress‐dependent manner and strongly suggests that it may be a useful therapeutic agent in colorectal carcinomas. Supported by CIHR.
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