The role of CFTR in regulating the cell cycle of intestinal stem cells

Abstract

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] [Abstract taken from public pdf.] Cystic fibrosis (CF) patients and CF mouse models have an increased risk for gastrointestinal (GI) cancer. Intestinal stem cells (ISCs) are thought to drive GI cancer potentially due to ISC abnormally rapid cell divisions or hyperproliferation. Elevated intracellular chloride can facilitate the transition of ISC from a resting state to a proliferating state. Previous studies have shown the CF epithelium sustains elevated intracellular chloride. Elevated intracellular chloride can result in a decrease in p21 expression, an important repressor of proliferation. It was concluded that Cftr regulates ISC proliferation.