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

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

Author information

1
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, United States.
2
Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, United States. Electronic address: donald_kufe@dfci.harvard.edu.

Abstract

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

PMID:
28302417
PMCID:
PMC5548633
DOI:
10.1016/j.bbcan.2017.03.003
[Indexed for MEDLINE]
Free PMC Article

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