MUC1: a novel metabolic master regulator.

Kamiya Mehla, Pankaj K Singh

Journal: Biochimica et biophysica acta 2014;1845(2):126-35

PMID: 24418575

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Abstract

MUC1, a type I transmembrane protein, is significantly overexpressed and aberrantly glycosylated in tumors of epithelial origin. By virtue of its aberrant signaling due to loss of apical-basal polarity in cancer, MUC1 regulates the metabolite flux at multiple levels. Serving as a transcriptional co-activator, MUC1 directly regulates expression of metabolic genes. By regulating receptor tyrosine kinase signaling, MUC1 facilitates production of biosynthetic intermediates required for cell growth. Also, via direct interactions, MUC1 modulates the activity/stability of enzymes and transcription factors that directly regulate metabolic functions. Additionally, by modulation of autophagy, levels of reactive oxygen species, and metabolite flux, MUC1 facilitates cancer cell survival under hypoxic and nutrient-deprived conditions. This article provides a comprehensive review of recent literature on novel metabolic functions of MUC1.

Address: The Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA.; The Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Genetic Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE 68198, USA; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

DOI: 10.1016/j.bbcan.2014.01.001

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https://assays.cancer.gov/CPTAC-146

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https://antibodies.cancer.gov/detail/CPTC-MUC1-1

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MeSH Terms: Autophagy, Cell Survival, Gene Expression Regulation, Neoplastic, Humans, Mucin-1, Neoplasms, Phosphorylation, Reactive Oxygen Species, Signal Transduction, Transcription Factors