TY - JOUR
T1 - MUC1
T2 - A novel metabolic master regulator
AU - Mehla, Kamiya
AU - Singh, Pankaj K.
N1 - Funding Information:
The authors thank Melody Montgomery and Dr. Laura Simone at UNMC for help in the professional editing of this manuscript. This work was supported in part by R01 ( R01 CA163649 , NCI) to P.K.S., American Association for Cancer Research (AACR)—Pancreatic Cancer Action Network (PanCAN) Career Development Award ( 30-20-25-SING ) to P.K.S., the Specialized Programs for Research Excellence (SPORE) Career Development Award ( P50 CA127297 , NCI) to P.K.S., SPORE Developmental Research Project Award ( P50 CA127297 , NCI) to P.K.S., Pancreatic Tumor Microenvironment Research network ( U54, CA163120 , NCI) to P.K.S., LB506 ( 2014-37 , DHHS-NE) to P.K.S., DOD BCRP Idea Award ( BC122040 , U.S. Army/USAMRAA/CDMRP) to P.K.S. and Cancer Prevention and Control Nutrition seed grant ( 15618 , GSCN) to P.K.S.
PY - 2014/4
Y1 - 2014/4
N2 - 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.
AB - 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.
KW - Cancer metabolism
KW - Glycolysis
KW - MUC1
KW - Nutrient stress and carbon flux
UR - http://www.scopus.com/inward/record.url?scp=84893189937&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84893189937&partnerID=8YFLogxK
U2 - 10.1016/j.bbcan.2014.01.001
DO - 10.1016/j.bbcan.2014.01.001
M3 - Article
C2 - 24418575
AN - SCOPUS:84893189937
SN - 0304-419X
VL - 1845
SP - 126
EP - 135
JO - Biochimica et Biophysica Acta - Reviews on Cancer
JF - Biochimica et Biophysica Acta - Reviews on Cancer
IS - 2
ER -