MUC1: A novel metabolic master regulator

Kamiya Mehla, Pankaj K. Singh

Research output: Contribution to journalArticlepeer-review

77 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)126-135
Number of pages10
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Issue number2
StatePublished - Apr 2014


  • Cancer metabolism
  • Glycolysis
  • MUC1
  • Nutrient stress and carbon flux

ASJC Scopus subject areas

  • Oncology
  • Genetics
  • Cancer Research


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