Paper published in “Biochimica et Biophysica Acta” describes how MUC1-C is involved in driving a program that integrates the induction of EMT with activation of stem cell traits, epigenetic reprogramming and immune evasion in human carcinomas.

The MUC1-C-integrated program provides support for the importance of this oncoprotein in cancer progression and emphasizes a critical need for developing agents against this widely overexpressed target in human malignancies.

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CITATION:

Biochim Biophys Acta. 2017 Mar 13. pii: S0304-419X(17)30023-9. doi: 10.1016/j.bbcan.2017.03.003. [Epub ahead of print]

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

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.
Copyright © 2017. Published by Elsevier B.V.

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