Targeting IL-17A: A New Frontier in the Treatment of Colitis-Associated Cancer

Ulcerative colitis (UC) is characterized by chronic inflammation in the colon that can lead to the development of colitis-associated cancer if left untreated. Interleukin-17A (IL-17A), an inflammatory cytokine produced by Th17 cells, plays a crucial role in mediating inflammatory reactions in autoimmune diseases like inflammatory bowel disease and has been implicated in colitis associated cancer development. This review discusses the importance of IL-17A in colitis associated cancer pathogenesis and examines novel therapies targeting IL-17A as potential treatments. Evidence from animal studies demonstrates that inhibition of IL-17A signaling can suppress intestinal inflammation and tumor development in colitis associated cancer models. Several natural compounds like cocoa, embelin, β-carotene, and melatonin have shown promise in reducing IL-17A expression and colitis associated cancer progression in preclinical studies. Additionally, administration of IL-17A antibodies has been found to decrease tumor formation in mouse models of colitis associated cancer. Recent research has also revealed the role of microRNAs like microRNA-146a in modulating IL-17 responses and limiting tumorigenic inflammation. While further research is needed, targeting the IL-17A pathway represents a promising therapeutic approach for preventing and treating colitis associated cancer. This review summarizes the current evidence supporting IL-17A as a key mediator of colitis associated cancer and highlights potential strategies to inhibit this pathway for therapeutic benefit.