Objective: In this review, we have summarized the influence of inflammation-related pathological mechanisms on the development of ulcerative colitis (UC) to colorectal cancer (CRC).
Background: UC is a chronic inflammatory bowel disease (IBD) of unknown etiology that affects the colon and rectum. Long-term inflammation of UC may greatly increase the risk of CRC, and the secretion of inflammatory factors and sustained inflammation may be key drivers of UC-associated CRC progression. Compared with the general population, the risk of CRC in patients with UC is 2.4 times higher, and the mortality rate of patients with UC is higher than that of those with sporadic CRC. The use of non-steroidal anti-inflammatory drugs can reduce the probability of UC transforming into CRC.
Methods: Literatures about inflammation and UC were extensively reviewed to analyze and discuss.
Conclusions: We believe that the mechanism of continuous inflammation that promotes cancer in UC may be the result of the mutual influence of intestinal microbes, inflammatory signals, and tissue remodeling. The invasion of intestinal microorganisms activates inflammatory signals and promotes the secretion of inflammatory factors which intensifies the remodeling of the extracellular matrix (ECM) and recruits immune cells. Eventually, a mutually engendering circuit of microbial invasion, release of inflammatory mediators, and remodeling of ECM is formed, which triggers continuous inflammation and promotes development of CRC.
Keywords: Crohn’s disease (CD); Ulcerative colitis (UC); gut microbes; inflammatory signals.