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The Heterogeneity of Lipid Metabolism in Cancer

  • Chapter
The Heterogeneity of Cancer Metabolism

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 1063))

  • 4032 Accesses

Abstract

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.

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Abbreviations

4-HNE:

4-Hydroxy-nonenal

ω-3/6:

Omega-3/6 fatty acid

ACC:

Acetyl-coenzyme A carboxylase

ACLY:

Adenosine triphosphate citrate lyase

ACSL3:

Acyl-coenzyme A synthetase long-chain family member 3

ACSS2:

Acyl-coenzyme A synthetase short-chain family member 2

AMPK:

Adenosine monophosphate-activated protein kinase

ATP:

Adenosine triphosphate

BMI:

Body mass index

BTA:

Benzene-tricarboxylate

CD36:

Cluster of differentiation 36 protein

CTP:

Citrate transporter protein

CoA:

Coenzyme A

CPT1:

Carnitine palmitoyltransferase 1

DNA:

Deoxyribonucleic acid

DNLS:

De novo lipid synthesis

EMT:

Epithelial-mesenchymal transition

ERS:

Endoplasmic reticulum stress

FADH2:

Flavin adenine dinucleotide

FAO:

Fatty acid oxidation

FAS:

Fatty acid synthase

FATP:

Fatty acid transport protein

GBM:

Glioblastoma multiforme

HFD:

High-fat diet

HMGCR:

3-Hydroxy-3-methylglutaryl-coenzyme A reductase

IDH:

Isocitrate dehydrogenase

LD:

Lipid droplet

LDL:

Low-density lipoprotein

LPL:

Lipoprotein lipase

NADH:

Nicotinamide adenine dinucleotide

NADPH:

Nicotinamide adenine dinucleotide phosphate

PE:

Phosphatidylethanolamine

PIP2:

Phosphatidylinositol-4,5-bisphosphate

PUFA:

Polyunsaturated fatty acid

ROS:

Reactive oxygen species

SCD:

Stearoyl-coenzyme A desaturase

TCA:

Tricarboxylic acid

TG:

Triglyceride

TME:

Tumor microenvironment

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Acknowledgments

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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Authors and Affiliations

  1. Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Joshua K. Park

  2. National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA

    Joshua K. Park & Nathan J. Coffey

  3. Department of Biological Sciences, Columbia University, New York, NY, USA

    Aaron Limoges

  4. Department of Pathology and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA

    Anne Le

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Correspondence to Anne Le .

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  1. Johns Hopkins Medicine, Baltimore, MD, USA

    Anne Le MD, HDR

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Park, J.K., Coffey, N.J., Limoges, A., Le, A. (2018). The Heterogeneity of Lipid Metabolism in Cancer. In: Le, A. (eds) The Heterogeneity of Cancer Metabolism. Advances in Experimental Medicine and Biology, vol 1063. Springer, Cham. https://doi.org/10.1007/978-3-319-77736-8_3

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