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Adipocyte and lipid metabolism in cancer drug resistance
Yihai Cao
Yihai Cao
Published July 2, 2019
Citation Information: J Clin Invest. 2019;129(8):3006-3017. https://doi.org/10.1172/JCI127201.
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Review

Adipocyte and lipid metabolism in cancer drug resistance

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Abstract

Development of novel and effective therapeutics for treating various cancers is probably the most congested and challenging enterprise of pharmaceutical companies. Diverse drugs targeting malignant and nonmalignant cells receive clinical approval each year from the FDA. Targeting cancer cells and nonmalignant cells unavoidably changes the tumor microenvironment, and cellular and molecular components relentlessly alter in response to drugs. Cancer cells often reprogram their metabolic pathways to adapt to environmental challenges and facilitate survival, proliferation, and metastasis. While cancer cells’ dependence on glycolysis for energy production is well studied, the roles of adipocytes and lipid metabolic reprogramming in supporting cancer growth, metastasis, and drug responses are less understood. This Review focuses on emerging mechanisms involving adipocytes and lipid metabolism in altering the response to cancer treatment. In particular, we discuss mechanisms underlying cancer-associated adipocytes and lipid metabolic reprogramming in cancer drug resistance.

Authors

Yihai Cao

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Figure 1

Mechanisms of cancer-associated adipocytes in tumor growth, metastasis, and cachexia.

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Mechanisms of cancer-associated adipocytes in tumor growth, metastasis, ...
Malignant cells produce various soluble and cell surface signaling molecules to reprogram metabolic activity and production of growth factors/cytokines in adipocytes through endocrine, paracrine, and juxtacrine signaling mechanisms. After receiving signals from malignant cells, cancer-associated adipocytes (CAAs) produce various growth factors, adipokines, and adipocytokines that directly affect tumor cell growth and invasion. Alternatively, the adipocyte-derived factors have a significant impact on nontumor cells in the tumor microenvironment to modulate tumor growth, metastasis, and cachexia. The tumor cell–triggered metabolic reprograming in adipocytes releases metabolic products such as free fatty acids (FFAs) that will be used as energy fuel molecules to support tumor growth and metastasis. Lipolysis is also one of the key processes causing adipose atrophy and cachexia in cancer patients.
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