Authors
Yuying Chen, Wen Liu, Bing Luo
Published in
Cell biochemistry and function. Volume 44. Issue 10. Pages e70314.
Abstract
AMP-activated protein kinase (AMPK), a key regulator of cellular energy metabolism, is activated under conditions of energy stress to restore metabolic homeostasis by promoting catabolic pathways and inhibiting anabolic processes such as lipid synthesis. Multiple key molecules involved in lipid metabolism are regulated by AMPK, and its role in cancer progression through lipid metabolism is dual-edged. On the one hand, AMPK suppresses lipogenesis by inhibiting key regulators such as SREBP, ACC, and HMGCR, thereby limiting the biosynthetic substrates and membrane lipid availability required for tumor cell proliferation. On the other hand, AMPK activation may also enhance fatty acid oxidation and metabolic adaptation, which can support growth and survival under nutrient limitation, hypoxia, or therapeutic stress. This dual role presents therapeutic challenges but also creates opportunities for context-specific intervention. In this review, we summarize the mechanisms by which AMPK regulates lipid metabolism in cancer and discuss the current progress, therapeutic potential, and limitations of AMPK-modulating strategies.
PMID:
42836364
Bibliographic data and abstract were imported from PubMed on 06 Oct 2026.
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