The Heterogeneity of Lipid Metabolism in Cancer

  • Joshua K. Park
  • Nathan J. Coffey
  • Aaron Limoges
  • Anne Le
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1063)


The study of cancer cell metabolism has traditionally focused on glycolysis and glutaminolysis. However, lipidomic technologies have matured considerably over the last decade and broadened our understanding of how lipid metabolism is relevant to cancer biology [1–3]. Studies now suggest that the reprogramming of cellular lipid metabolism contributes directly to malignant transformation and progression [4, 5]. For example, de novo lipid synthesis can supply proliferating tumor cells with phospholipid components that comprise the plasma and organelle membranes of new daughter cells [6, 7]. Moreover, the upregulation of mitochondrial β-oxidation can support tumor cell energetics and redox homeostasis [8], while lipid-derived messengers can regulate major signaling pathways or coordinate immunosuppressive mechanisms [9–11]. Lipid metabolism has therefore become implicated in a variety of oncogenic processes, including metastatic colonization, drug resistance, and cell differentiation [10, 12–16]. However, whether we can safely and effectively modulate the underlying mechanisms for cancer therapy is still an open question.


Cancer metabolism Tumor heterogeneity Lipid synthesis Fatty acid oxidation Fatty acid uptake Metastasis Lipidomics 





Omega-3/6 fatty acid


Acetyl-coenzyme A carboxylase


Adenosine triphosphate citrate lyase


Acyl-coenzyme A synthetase long-chain family member 3


Acyl-coenzyme A synthetase short-chain family member 2


Adenosine monophosphate-activated protein kinase


Adenosine triphosphate


Body mass index




Cluster of differentiation 36 protein


Citrate transporter protein


Coenzyme A


Carnitine palmitoyltransferase 1


Deoxyribonucleic acid


De novo lipid synthesis


Epithelial-mesenchymal transition


Endoplasmic reticulum stress


Flavin adenine dinucleotide


Fatty acid oxidation


Fatty acid synthase


Fatty acid transport protein


Glioblastoma multiforme


High-fat diet


3-Hydroxy-3-methylglutaryl-coenzyme A reductase


Isocitrate dehydrogenase


Lipid droplet


Low-density lipoprotein


Lipoprotein lipase


Nicotinamide adenine dinucleotide


Nicotinamide adenine dinucleotide phosphate






Polyunsaturated fatty acid


Reactive oxygen species


Stearoyl-coenzyme A desaturase


Tricarboxylic acid




Tumor microenvironment



We thank Dr. Resat Cinar, PhD, MBA, for his support and Mr. Daniel C. McCaskey, JD, for his review of the manuscript.


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Joshua K. Park
    • 1
    • 2
  • Nathan J. Coffey
    • 2
  • Aaron Limoges
    • 3
  • Anne Le
    • 4
  1. 1.Department of PathologyJohns Hopkins University School of MedicineBaltimoreUSA
  2. 2.National Institute on Alcohol Abuse and Alcoholism, National Institutes of HealthBethesdaUSA
  3. 3.Department of Biological SciencesColumbia UniversityNew YorkUSA
  4. 4.Department of Pathology and OncologyJohns Hopkins University School of MedicineBaltimoreUSA

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