title: MUC1-C Oncoprotein Integrates a Program of EMT, Epigenetic Reprogramming and Immune Evasion in Human Carcinomas.
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.
authors.affiliation: Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, United States.
authors.forename: Hasan
authors.initials: H
authors.lastname: Rajabi
authors.affiliation: Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, United States. Electronic address: donald_kufe@dfci.harvard.edu.
authors.forename: Donald
authors.initials: D
authors.lastname: Kufe
mesh_terms: D000818:Animals; D002277:Carcinoma / Q000235:genetics*; D044127:Epigenesis, Genetic / Q000235:genetics*; D058750:Epithelial-Mesenchymal Transition / Q000235:genetics*; D006801:Humans; D057131:Immune Evasion / Q000235:genetics*; D018396:Mucin-1 / Q000235:genetics*; D015513:Oncogene Proteins / Q000235:genetics*
chemical_list: D018396:Mucin-1; D015513:Oncogene Proteins
keywords: BMI1; DNMTs; EMT; MUC1-C; PD-L1; epigenetics; immune evasion; tumor suppressor genes