The AMP-activated protein kinase (AMPK) and cancer: many faces of a metabolic regulator

Brandon Faubert, Emma E Vincent, Maya C Poffenberger, Russell G Jones

Research output: Contribution to journalArticle (Academic Journal)peer-review

271 Citations (Scopus)


The AMP-activated protein kinase (AMPK) is a central regulator of cellular metabolism and energy homeostasis in mammalian tissues. Pertinent to cancer biology is the fact that AMPK is situated in the center of a signaling network involving established tumor suppressors including LKB1, TSC2 and p53. However, recent research suggests that AMPK can exert pro- or anti-tumorigenic roles in cancer depending on context. Loss of AMPK activity has been observed in several tumor types, and can cooperate with oncogenic drivers to reprogram tumor cell metabolism and enhance cell growth and proliferation. However, AMPK activation can also provide a growth advantage to tumor cells by regulating cellular metabolic plasticity, thus providing tumor cells the flexibility to adapt to metabolic stress. Here we discuss the contextual nature of the "two faces" of AMPK in cancer, and discuss the rationale and context for employing AMPK activators versus inhibitors for cancer therapy.

Original languageEnglish
Pages (from-to)165-70
Number of pages6
JournalCancer Letters
Issue number2 Pt A
Publication statusPublished - 28 Jan 2015


  • AMP-Activated Protein Kinases
  • Biguanides
  • Cell Proliferation
  • Energy Metabolism
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • Neoplasms
  • Oxidative Stress
  • Protein-Serine-Threonine Kinases
  • Signal Transduction
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins
  • Journal Article
  • Research Support, Non-U.S. Gov't
  • Review


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