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Breast Cancer and Lipid Metabolism

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Lipidomics in Health & Disease

Part of the book series: Translational Bioinformatics ((TRBIO,volume 14))

Abstract

Alteration of lipid metabolism plays a critical role in the development of many types of cancer including breast cancer. Lipid metabolism can be regulated by a variety of signaling pathways with proliferative stimuli, apoptotic stimuli or environment changes under physiological, pathophysiological or therapeutic conditions. On the other hand, many lipids and lipid intermediate metabolites are also important signaling molecules involved in cell signaling that regulate cell proliferation, differentiation, apoptosis and migration as well as responses to drug treatment. In physiological condition, lipid metabolism (anabolism and catabolism) is tightly regulated by signaling network in the cell under designed path to growth, proliferation, differentiation and migration. Dysregulation of lipid metabolism under pathological condition leads to alteration of lipid profiles and accumulation of some “bad” lipids which can cause cell overgrowth and hyper-proliferation such as cancer and cell death such as tissue injury (Fig. 8.3). This chapter focuses on the emerging understanding of the role of lipid metabolic pathway in breast carcinogenesis and tumor progression. The update information indicates that the modulation of lipid metabolism can potentially be exploited to prevent breast cancer and enhance efficacy of breast cancer therapy.

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Abbreviations

ChoK:

Choline kinase

DG:

diacylglycerol

ER:

estrogen receptor

FAS:

fatty acid synthase

FIPI:

5-Fluoro-2-indolyl des-chlorohalopemide

HER:

human epidermal growth factor receptor

HMG-CoA:

3-hydroxyl-3-methyl glutaryl-coenzyme A

HMGCR:

3-hydroxyl-3-methyl glutaryl-coenzyme A reductase

JNK:

c-Jun N-terminal kinase

LPA:

lysophosphatidic acid

LPC:

lysophosphatidylcholine

LXR:

liver X receptors

MAPK:

mitogen-activated protein kinases

PA:

phosphatidic acid

PC:

phosphatidylcholine

PE:

phosphatidylethanolamine

PG:

phosphatidylglycerol

PI:

phosphatidylinositol

PI-3-K:

PI-3-kinase

PI-3-P:

PI-3-phoshpate

PI-3,4-P2:

PI-3,4-phoshpates

PI-3,4,5-P3:

PI-3,4,5-phoshpates

PLD:

phospholipase D

PR:

progesterone receptor

PUFA:

polyunsaturated fatty acids

ROS:

reactive oxygen species

SFA:

saturated fatty acids

SPM:

sphingomyelin

SREBP:

sterol regulatory element binding protein

TG:

triacylglycerol

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Authors and Affiliations

  1. Division of Hematology/Oncology, Department of Internal Medicine, School of Medicine, Saint Louis University, Saint Louis, MO, USA

    Chunfa Huang, Yifan Tu & Carl E. Freter

  2. Department of Surgery of the Fourth Hospital, Hebei Medical University, Shijiazhuang, Hebei, People’s Republic of China

    Yuntao Li

Authors
  1. Chunfa Huang
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  2. Yuntao Li
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  3. Yifan Tu
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  4. Carl E. Freter
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Corresponding author

Correspondence to Chunfa Huang .

Editor information

Editors and Affiliations

  1. Zhongshan Hospital Institute of Clinical Science, Fudan University Shanghai Medical College, Shanghai, China

    Xiangdong Wang

  2. Zhongshan Hospital Institute of Clinical Science, Fudan University Shanghai Medical School, Shanghai, China

    Duojiao Wu

  3. Institutes of Biomedicine, Fudan University, Shanghai, China

    Huali Shen

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© 2018 Springer Nature Singapore Pte Ltd.

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Huang, C., Li, Y., Tu, Y., Freter, C.E. (2018). Breast Cancer and Lipid Metabolism. In: Wang, X., Wu, D., Shen, H. (eds) Lipidomics in Health & Disease. Translational Bioinformatics, vol 14. Springer, Singapore. https://doi.org/10.1007/978-981-13-0620-4_8

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