Leptin enhances STAT-3 phosphorylation in HC11 cell line: Effect on cell differentiation and cell viability

Massimiliano Motta, Paolo Accornero, Riccardo Taulli, Paola Bernabei, Sylvane Desrivières, Mario Baratta

Research output: Contribution to journalArticlepeer-review

Abstract

Leptin is produced in the mammary gland by the fat tissue or by the mammary epithelium. The aim of this study was to investigate the role of leptin on mammary epithelial cell differentiation and cell viability. This study was conducted using the mouse mammary epithelial cell line HC11. We show that leptin, synergizes with prolactin to increase β-casein gene expression during mammary epithelial cell differentiation. This was correlated with increased phosphorylation of the signal transducer and activator of transcription 3 (STAT-3). Inactivating the function of STAT-3 by expression of a short hairpin RNA demonstrated that the effect of leptin on β-casein expression is mediated by STAT-3. Secondarly, cells in which STAT-3 had been inactivated showed increased cell viability compared to controls and were resistant to the negative effect mediated by leptin. Further, leptin triggers apoptosis in mammary epithelial cells cultivated in non-differentiating conditions. Taken together, these results suggest that leptin, by activating STAT-3, may act as a paracrine factor modulating mammary epithelial cell function.

Original languageEnglish
Pages (from-to)149-155
Number of pages7
JournalMolecular and Cellular Endocrinology
Volume263
Issue number1-2
DOIs
Publication statusPublished - Jan 15 2007

Keywords

  • β-Casein
  • Cell viability
  • Differentiation
  • Leptin
  • Mammary epithelial cell
  • STAT-3

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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