| Literature DB >> 28302417 |
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.Entities:
Keywords: BMI1; DNMTs; EMT; MUC1-C; PD-L1; epigenetics; immune evasion; tumor suppressor genes
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Year: 2017 PMID: 28302417 PMCID: PMC5548633 DOI: 10.1016/j.bbcan.2017.03.003
Source DB: PubMed Journal: Biochim Biophys Acta Rev Cancer ISSN: 0304-419X Impact factor: 10.680