MUC1: A novel metabolic master regulator

被引:78
作者
Mehla, Kamiya [1 ]
Singh, Pankaj K. [1 ,2 ,3 ,4 ]
机构
[1] Univ Nebraska Med Ctr, Fred & Pamela Buffett Canc Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA
[2] Univ Nebraska Med Ctr, Dept Biochem & Mol Biol, Omaha, NE 68198 USA
[3] Univ Nebraska Med Ctr, Dept Genet Cell Biol & Anat, Omaha, NE 68198 USA
[4] Univ Nebraska Med Ctr, Dept Pathol & Microbiol, Omaha, NE 68198 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER | 2014年 / 1845卷 / 02期
关键词
MUC1; Cancer metabolism; Glycolysis; Nutrient stress and carbon flux; HYPOXIA-INDUCIBLE FACTOR-1; FATTY-ACID SYNTHASE; BREAST-CANCER; MEMBRANE GLYCOPROTEIN; PROTEIN EXPRESSION; SURVIVAL RESPONSE; LIPID-METABOLISM; TUMOR-CELLS; ONCOPROTEIN; GENE;
D O I
10.1016/j.bbcan.2014.01.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
MUCI, 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. (c) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:126 / 135
页数:10
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