MUC1-C in chronic inflammation and carcinogenesis; emergence as a target for cancer treatment

Carcinogenesis. 2020 Sep 24;41(9):1173-1183. doi: 10.1093/carcin/bgaa082.


Chronic inflammation is a highly prevalent consequence of changes in environmental and lifestyle factors that contribute to the development of cancer. The basis for this critical association has largely remained unclear. The MUC1 gene evolved in mammals to protect epithelia from the external environment. The MUC1-C subunit promotes responses found in wound healing and cancer. MUC1-C induces EMT, epigenetic reprogramming, dedifferentiation and pluripotency factor expression, which when prolonged in chronic inflammation promote cancer progression. As discussed in this review, MUC1-C also drives drug resistance and immune evasion, and is an important target for cancer therapeutics now under development.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology*
  • Carcinogenesis / drug effects*
  • Carcinogenesis / metabolism
  • Carcinogenesis / pathology
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / metabolism
  • Inflammation / pathology
  • Mucin-1 / genetics
  • Mucin-1 / metabolism*
  • Neoplasms / drug therapy*
  • Neoplasms / metabolism
  • Neoplasms / pathology


  • Antineoplastic Agents
  • Mucin-1