Immunological Mechanisms in Inflammation-Associated Colon Carcinogenesis

Int J Mol Sci. 2020 Apr 26;21(9):3062. doi: 10.3390/ijms21093062.


Patients with chronic inflammatory bowel diseases are at an increased risk of developing colitis-associated cancer (CAC). Chronic inflammation positively correlates with tumorigenesis. Similarly, the cumulative rate of incidence of developing CAC increases with prolonged colon inflammation. Immune signaling pathways, such as nuclear factor (NF)-κB, prostaglandin E2 (PGE2)/cyclooxygenase-2 (COX-2), interleukin (IL)-6/signal transducer and activator of transcription 3 (STAT3), and IL-23/T helper 17 cell (Th17), have been shown to promote CAC tumorigenesis. In addition, gut microbiota contributes to the development and progression of CAC. This review summarizes the signaling pathways involved in the pathogenesis following colon inflammation to understand the underlying molecular mechanisms in CAC tumorigenesis.

Keywords: colitis-associated cancer; colorectal cancer; inflammatory bowel disease; signaling pathway; ulcerative colitis.

Publication types

  • Review

MeSH terms

  • Animals
  • Colonic Neoplasms / etiology
  • Colonic Neoplasms / immunology*
  • Cyclooxygenase 2 / metabolism
  • Cytokines / metabolism
  • Disease Progression
  • Dysbiosis / complications*
  • Dysbiosis / immunology
  • Gastrointestinal Microbiome
  • Humans
  • Inflammatory Bowel Diseases / complications*
  • Inflammatory Bowel Diseases / immunology
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction
  • Th17 Cells / metabolism


  • Cytokines
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • Cyclooxygenase 2
  • PTGS2 protein, human