Immune/inflammatory cells infiltrate almost all human solid tumors and affect all stages of carcinogenesis as they produce different cytokine subsets. The overproduction of TH17 cytokines marks the early stages of colorectal carcinoma (CRC) and negatively influences the prognosis of CRC patients. Studies with murine models of CRC have delineated the mechanisms by which TH17 cytokines, notably, interleukin (IL)-17A, IL-17F, IL-21, and IL-22, regulate oncogenesis and tumor progression, paving the way to the development of novel anticancer drugs. In this review article, we discuss experimental data supporting the role of TH17 cytokines in the modulation of colorectal tumorigenesis.
Keywords: IL-17A; IL-17F; IL-21; IL-22; NFκB; STAT3; TH17 cells; anti-cytokine therapy; colitis-associated colon cancer; inflammation.