Full text is available at the source.
Non-hematopoietic STAT6 induces epithelial tight junction dysfunction and promotes intestinal inflammation and tumorigenesis
STAT6 outside blood cells disrupts gut lining, leading to inflammation and tumor growth
AI simplified
Abstract
STAT6 activation was detected in inflamed colonic epithelium of active IBD patients.
- Non-hematopoietic STAT6 triggered DSS-induced colitis and tumor development.
- STAT6 may enhance gut permeability and microbiota translocation by disrupting epithelial tight junctions.
- Long-myosin light-chain kinase (MLCK1) is a target of STAT6 that contributes to tight junction dysfunction.
- Neutralization of IL-13 improved gut permeability and reduced DSS-induced colitis by inhibiting epithelial STAT6 activation.
- Pharmacological inhibition of STAT6 reduced intestinal tumor formation in mice.
- Tumoral p-STAT6 levels are positively correlated with clinical stage and poor prognosis in human colorectal cancer.
AI simplified