Leptin (Obesity Protein) and Breast Cancer Metastasis
Abstract
Obesity in the United States has reached the alarming rate of -60% and is considered a second, after smoking, major killer. The link between obesity and breast cancer development has been postulated but the molecular mechanisms involved are not clear (1). Leptin, a 16 kDa protein product of the OB (obesity) gene is a cytokine reported to be secreted mainly from adipocytes and has been shown to control body fat mass and food intake by providing information to the central nervous system (2). The abundance of leptin is greater in females than in males and is regulated by steroid hormones and growth factors, such as estradiol, insulin and insulin-like growth factor 1(3-7). The levels of these substances are elevated in individuals with upper body obesity. This type of obesity correlates with increased breast cancer risk in post-menopausal women (1). In addition to its role as a regulator of appetite and metabolism, leptin can be involved in other processes, such as hematopoiesis, reproduction, and immunity (2,7) Recently, it has been demonstrated that leptin can act as a mitogen, chemoattractant, and angiogenic factor in different cell models (8-12). New data documented that human breast cancer cell lines and breast tumors may express leptin and leptin receptor (Ob-R) (8,9,13) In addition, leptin has been show to induce DNA synthesis in MCF-7 and T47D breast cancer cell lines (8,9). We hypothesized that in obese women, locally elevated levels of estrogens and insulin might increase the synthesis of leptin in adipocytes and/or epithelial cells, in effect leading to increased proliferation and/or migration in primary breast tumor.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2002
- Accession Number
- ADA407425
Entities
People
- Eva Surmacz
Organizations
- Thomas Jefferson University