Chronic leptin treatment sensitizes MCF-7 breast cancer cells to estrogen

Cell Physiol Biochem. 2011;28(5):823-32. doi: 10.1159/000335796. Epub 2011 Dec 15.

Abstract

Background/aims: Obesity is associated with an increased risk of estrogen-dependent breast cancer. The adipokine leptin, whose levels are chronically increased in obese people, has been shown to stimulate ER positive cancer cell growth. Considering previous evidence of a crosstalk between leptin and estrogen signaling, the objective of this study was to establish the influence of chronic leptin treatment on estrogen-dependent cell growth.

Methods: To this aim, we use the estrogen receptor (ER) positive MCF-7 breast cancer cell line treated chronically with leptin and analyzed estrogen-dependent cell growth, ERs (ERα and ERβ) expression, ER-dependent transcriptional activity as well as cell survival to the antiestrogenic agents tamoxifen and ICI 182,780.

Results: Leptin signaling pathway kept activated after chronic stimulation (7 days) with leptin showing significant phosphorylation of JAK2 and STAT3 and higher cell proliferation rate. Chronic leptin at 100 ng/mL dose increased ERα to ERβ ratio and consistently enhanced estrogen-dependent transcriptional activity, increasing E2-dependent cell growth and resistance to antiestrogen agents.

Conclusion: This study supports the existence of a crosstalk between leptin and estrogen, in which leptin might play an important role potentiating the mitogenic action of estrogen, probably by alteration of ERα to ERβ ratio.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Breast Neoplasms / pathology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Estradiol / analogs & derivatives
  • Estradiol / pharmacology
  • Estrogen Receptor alpha / metabolism
  • Estrogen Receptor beta / metabolism
  • Estrogens / metabolism*
  • Female
  • Fulvestrant
  • Humans
  • Janus Kinase 2 / metabolism
  • Leptin / pharmacology*
  • Phosphorylation
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects
  • Tamoxifen / pharmacology

Substances

  • Antineoplastic Agents
  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Estrogens
  • Leptin
  • STAT3 Transcription Factor
  • Tamoxifen
  • Fulvestrant
  • Estradiol
  • Janus Kinase 2