Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume 1831, Issue 10, Pages 1533-1541Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbalip.2013.02.010
Keywords
Obesity; Adipocytes; Visceral adipose tissue; Cancer; Metastasis; Metabolic symbiosis
Funding
- National Cancer Institute
- Reproductive Scientist Development Program
- Prevent Cancer Foundation
- UPCI
- Pennsylvania Department of Health, PA CURE
- Clinical Scientist Award in Translational Research from the Burroughs Wellcome Fund
- Ovarian Cancer Research Fund
- Bears Care, the charitable beneficiary of the Chicago Bears Football Club
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Adipose tissue influences tumor development in two major ways. First, obese individuals have a higher risk of developing certain cancers (endometrial, esophageal, and renal cell cancer). However, the risk of developing other cancers (melanoma, rectal, and ovarian) is not altered by body mass. In obesity, hypertrophied adipose tissue depots are characterized by a state of low grade inflammation. In this activated state, adipocytes and inflammatory cells secrete adipokines and cytokines which are known to promote tumor development. In addition, the adipocyte mediated conversion of androgens to estrogen specifically contributes to the development of endometrial cancer, which shows the greatest relative risk (6.3-fold) increase between lean and obese individuals. Second, many tumor types (gastric, breast, colon, renal, and ovarian) grow in the anatomical vicinity of adipose tissue. During their interaction with cancer cells, adipocytes dedifferentiate into pre-adipocytes or are reprogrammed into cancer-associated adipocytes (CAA). CAA secrete adipokines which stimulate the adhesion, migration, and invasion of tumor cells. Cancer cells and CAA also engage in a dynamic exchange of metabolites. Specifically, CAA release fatty acids through lipolysis which are then transferred to cancer cells and used for energy production through beta-oxidation. The abundant availability of lipids from adipocytes in the tumor microenvironment, supports tumor progression and uncontrolled growth. Given that adipocytes are a major source of adipokines and energy for the cancer cell, understanding the mechanisms of metabolic symbiosis between cancer cells and adipocytes, should reveal new therapeutic possibilities. This article is part of a Special Issue entitled lipid Metabolism in Cancer. (C) 2013 Elsevier B.V. All rights reserved.
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