Abstract
Chronic inflammation characterizing patients with inflammatory bowel disease (IBD) represents a major risk factor for the development of colorectal cancer. Mechanisms underlying this neoplastic transformation are not fully understood though studies in experimental models of colon carcinogenesis suggest that inflammatory cell-derived cytokines either directly or indirectly stimulate the uncontrolled growth of cancer cells. Nevertheless, under specific inflammatory conditions, immune cells can boost an anti-tumor immune response with the down-stream effect of eliminating dysplastic and cancerous cells. This review outlines the beneficial and detrimental role of inflammation in colon carcinogenesis.
Highlights
Chronic inflammation is supposed to be a driving force for the growth of many human cancers [1].This is for example evident in patients with ulcerative colitis (UC) and patients with Crohn’s disease (CD), the two major forms of inflammatory bowel disease (IBD) in humans
There is no conclusive evidence that Type II natural killer T (NKT) cells contribute to colitis-associated colorectal cancer (CRC), it is tempting to speculate that activation of this cell subset in course of colitis may contribute to colon carcinogenesis by both dampening the host anti-tumor response and amplifying the ongoing inflammation
Fukata and coworkers report that TLR4 is over-expressed in UC-associated CRC and, by using the AOM + dextran sodium sulfate (DSS) mouse model, these authors showed that TLR4-deficient mice are largely protected against the development of tumors as compared to wild-type mice [39]
Summary
Chronic inflammation is supposed to be a driving force for the growth of many human cancers [1] This is for example evident in patients with ulcerative colitis (UC) and patients with Crohn’s disease (CD), the two major forms of inflammatory bowel disease (IBD) in humans. The regulatory effects of inflammatory cells on the growth and survival of cancer cells are in part dependent on the synthesis of cytokines, which can either directly or indirectly target CRC cells and modulate their behavior. Cytokines such as interleukin (IL)-6, IL-17A, IL-21 and tumor necrosis factor (TNF)-α contribute to the formation of a tumor-supportive microenvironment, while interferon (IFN)-γ is supposed to exert tumor-suppressive functions [8]. We discuss the beneficial and detrimental role of gut inflammation in the growth of CRC cells
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