期刊
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER
卷 1845, 期 2, 页码 126-135出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbcan.2014.01.001
关键词
MUC1; Cancer metabolism; Glycolysis; Nutrient stress and carbon flux
资金
- NCI [R01 CM 63649,]
- American Association for Cancer Research (AACR)-Pancreatic Cancer Action Network (PanCAN) Career Development Award [30-20-25-SING]
- Specialized Programs for Research Excellence (SPORE) Career Development Award (NCI) [P50 CA127297]
- SPORE Developmental Research Project Award (NCI) [P50 CA127297]
- Pancreatic Tumor Microenvironment Research network (NCI) [U54, CA163120]
- DHHS-NE [LB506 (2014-3)]
- DOD BCRP Idea Award [BC122040]
- U.S. Army/USAMRAA/CDMRP)
- Cancer Prevention and Control Nutrition seed grant (GSCN) [15618]
- CDMRP [BC122040, 542317] Funding Source: Federal RePORTER
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.
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