AMPK: opposing the metabolic changes in both tumour cells and inflammatory cells?

Madhumita Dandapani, D. Grahame Hardie (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    36 Citations (Scopus)

    Abstract

    AMPK (AMP-activated protein kinase) is a sensor of cellular energy status that appears to have arisen during early eukaryotic evolution. In the unicellular eukaryote Saccharomyces cerevisiae, the AMPK orthologue is activated by glucose starvation and is required for the switch from glycolysis (fermentation) to oxidative metabolism when glucose runs low. In mammals, rapidly proliferating cells (including tumour cells) and immune cells involved in inflammation both tend to utilize rapid glucose uptake and glycolysis (termed the Warburg effect or aerobic glycolysis) rather than oxidative metabolism to satisfy their high demand for ATP. Since mammalian AMPK, similar to its yeast orthologue, tends to promote the more energy-efficient oxidative metabolism at the expense of glycolysis, it might be expected that drugs that activate AMPK would inhibit cell proliferation and and hence cancer, as well as exerting anti-inflammatory effects. Evidence supporting this view is discussed, including our findings that AMPK is activated by the classic anti-inflammatory drug salicylate.

    Original languageEnglish
    Pages (from-to)687-693
    Number of pages7
    JournalBiochemical Society Transactions
    Volume41
    Issue number2
    Early online date21 Mar 2013
    DOIs
    Publication statusPublished - Apr 2013

    Keywords

    • ENERGY SENSOR
    • inflammation
    • metabolism
    • AMP-activated protein kinase (AMPK)
    • PHOSPHORYLATION
    • CANCER
    • SKELETAL-MUSCLE
    • LKB1
    • ACTIVATED PROTEIN-KINASE
    • CARBOXYLATION
    • GROWTH
    • innate immunity
    • YEAST SNF1
    • cancer
    • INHIBITION

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