Lipid Metabolism in Cancer Pathophysiology
Summary
Cancer cells reprogram lipid metabolism to fulfil increased demands for membrane synthesis, energy production and signalling. Alterations encompass enhanced uptake of exogenous fatty acids, up-regulated de novo lipogenesis and adaptive changes in lipid storage and oxidation. Central regulators include sterol regulatory element-binding proteins (SREBPs), which integrate oncogenic signals to drive fatty acid and cholesterol synthesis, and enzymatic networks that modulate lipid composition to maintain redox balance and support rapid proliferation. Crosstalk between cancer cells and the tumour microenvironment further shapes lipid availability and inflammatory responses, while metabolic plasticity enables adaptation to nutrient stress. Disrupted lipid homeostasis thus underpins key hallmarks of malignancy, offering biomarkers for disease progression and actionable targets for therapy.
Research from Nature Portfolio
Recent studies have elucidated the role of palmitic acid as a molecular checkpoint in hepatocellular carcinoma cells, showing that its conversion into palmitoyl-coenzyme A enables the palmitoylation of a plant homeodomain finger protein, promoting its ubiquitin-dependent degradation. This loss of a tumour suppressor enhances the stability and activity of a master lipogenic transcription factor, thereby amplifying fatty acid synthesis. The findings link dietary palmitic acid levels to intratumoural lipid reprogramming and suggest that modulating palmitoylation pathways may represent a novel approach to restrain tumour growth.
Lipid Metabolism in Cancer Pathophysiology publication trend
The graph below shows the total number of articles in lipid metabolism in cancer pathophysiology across all publications each year (not limited to Nature Index journals).
Technical terms
Palmitoylation: Covalent attachment of palmitic acid to proteins, modulating their localisation and turnover.
SREBP1c: A membrane-bound transcription factor that activates genes required for fatty acid and triglyceride synthesis.
Ubiquitination: Conjugation of ubiquitin to proteins, marking them for proteasomal degradation.
Lipogenesis: Pathway converting acetyl-CoA into fatty acids for membrane assembly and energy storage.
Branched-chain fatty acids (BCFA): Fatty acids featuring methyl branches, involved in membrane fluidity and signalling.
Lipid reprogramming: Adaptive remodelling of lipid metabolic pathways by cancer cells to support proliferation and survival.
References
- Palmitoylation-driven PHF2 ubiquitination remodels lipid metabolism through the SREBP1c axis in hepatocellular carcinoma. Nature Communications (2023).
- Monomethyl branched-chain fatty acids: Health effects and biological mechanisms. Progress in Lipid Research (2023).
- Sterol regulatory element binding protein-dependent regulation of lipid synthesis supports cell survival and tumor growth. Cancer & Metabolism (2013).
- Changes in lipids composition and metabolism in colorectal cancer: a review. Lipids in Health and Disease (2019).
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