MUC1-C Oncoprotein Integrates a Program of EMT, Epigenetic Reprogramming and Immune Evasion in Human Carcinomas

Biochim Biophys Acta Rev Cancer. 2017 Aug;1868(1):117-122. doi: 10.1016/j.bbcan.2017.03.003. Epub 2017 Mar 14.


The MUC1 gene evolved in mammalian species to provide protection of epithelia. The transmembrane MUC1 C-terminal subunit (MUC1-C) signals stress to the interior of the epithelial cell and, when overexpressed as in most carcinomas, functions as an oncoprotein. MUC1-C induces the epithelial-mesenchymal transition (EMT) by activating the inflammatory NF-κB p65 pathway and, in turn, the EMT-transcriptional repressor ZEB1. Emerging evidence has indicated that MUC1-C drives a program integrating the induction of EMT with activation of stem cell traits, epigenetic reprogramming and immune evasion. This mini-review focuses on the potential importance of this MUC1-C program in cancer progression.

Keywords: BMI1; DNMTs; EMT; MUC1-C; PD-L1; epigenetics; immune evasion; tumor suppressor genes.

Publication types

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

MeSH terms

  • Animals
  • Carcinoma / genetics*
  • Epigenesis, Genetic / genetics*
  • Epithelial-Mesenchymal Transition / genetics*
  • Humans
  • Immune Evasion / genetics*
  • Mucin-1 / genetics*
  • Oncogene Proteins / genetics*


  • Mucin-1
  • Oncogene Proteins