Critical signaling pathways governing colitis-associated colorectal cancer: Signaling, therapeutic implications, and challenges

Abstract

Long-term colitis in people with inflammatory bowel disease (IBD) may lead to colon cancer called colitis-associated colorectal cancer (CAC). Since the advent of preclinical prototypes of CAC, various immunological messaging cascades have been identified as implicated in developing this disease. The toll-like receptor (TLR)s, Janus kinase (JAK)-signal transducer and activator of transcription (STAT), Nuclear factor-kappa B (NF-κB), mammalian target of rapamycin complex (mTOR), autophagy, and oxidative stress are only a few of the molecular mechanisms that have been recognized as major components to CAC progression. These pathways may also represent attractive medicinal candidates for the prevention and management of CAC. CAC signaling mechanisms at the molecular level and how their dysregulation may cause illness are summarized in this comprehensive overview.

Keywords: Colitis; Colorectal cancer; Crohn's disease; IBD; Signaling.