Leptin (Obesity Protein) and Breast Cancer Metastasis

Abstract

Obesity is a risk factor for breast cancer in postmenopausal% women. Adipose tissue is a major source of leptin, a cytokine acting as a key regulator of energy balance. Leptin can also induce mitogenic and angiogenic effects in different cell types. New data suggested that in breast cancer cells, leptin can stimulate proliferation by activating the long form of the Ob receptor (ObR). We hypothesized that in obese women, locally elevated levels of leptin could promote the growth of primary breast tumors. The results of our work indicated that 1) several breast cancer cell lines express the long and short form of the leptin receptor (Ob-R); 2) leptin stimulates the proliferation in different breast cancer cell lines by 30- 40%; 3) in MCF-7 cells, leptin activates the ERKl/2 and STAT3 signaling pathways; 4) in MCF-7 cells, leptin interferes with the action of the antiestrogen ICI 182,780 by upregulating the activity of estrogen receptor alpha. In summary, our data suggested that higher levels of leptin could promote breast cancer cells growth and impede the efficacy of hormonal treatments.

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Document Details

Document Type
Technical Report
Publication Date
Aug 01, 2003
Accession Number
ADA418984

Entities

People

  • Eva Surmacz

Organizations

  • Thomas Jefferson University

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Abstracts
  • Biomedical Research
  • Breast Cancer
  • Cancer
  • Cell Line
  • Cells
  • Cytokines
  • Estrogens
  • Growth Factors
  • Hormones
  • Mammary Glands
  • Metastasis
  • Neoplasms
  • Proteins
  • Regulators
  • Tumor Cell Line
  • United States

Fields of Study

  • Medicine

Readers

  • Breast cancer cell signaling and growth regulation.
  • Molecular and Cellular Biology