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SOCS3 promotes apoptosis of mammary differentiated cells

Fabienne Le Provost1, Keiko Miyoshi, Jean-Luc Vilotte

  • 1Laboratory of Genetics and Physiology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. Fabienne.LeProvost@jouy.inra.fr

Biochemical and Biophysical Research Communications
|November 18, 2005
PubMed

Insights

Suppressor of cytokine signaling 3 (SOCS3) regulates mammary gland development by promoting apoptosis in adipocytes and epithelial cells. Prolactin stimulates SOCS3 expression in stromal cells, independent of STAT5a.

Area of Science:

  • Molecular Endocrinology
  • Developmental Biology
  • Cell Signaling

Background:

  • Mammary gland development and function are regulated by cytokines and modulated by suppressor of cytokine signaling (SOCS) proteins.
  • In vitro studies show SOCS3 inhibits prolactin (PRL)-induced milk protein gene expression and STAT5 activation.

Purpose of the Study:

  • To investigate the expression pattern of SOCS3 during mouse mammary gland development.
  • To determine the regulation of SOCS3 by PRL and growth hormone (GH) in wild-type and STAT5a-null mammary tissue.

Main Methods:

  • Analysis of SOCS3 expression in mouse mammary tissue during development.
  • Investigation of SOCS3 regulation by PRL and GH in wild-type and STAT5a-null models.
  • Assessment of STAT5 and STAT3 activation.

Main Results:

  • In vivo, PRL stimulates SOCS3 expression in stromal adipocytes independently of STAT5a.
  • In mammary epithelial cells, SOCS3 expression correlates with STAT3 activation.
  • SOCS3 expression is observed in adipocytes during gestation and epithelial cells during involution.

Conclusions:

  • SOCS3 plays a role in mammary gland involution by promoting apoptosis of differentiated adipocytes.
  • SOCS3 contributes to the apoptosis of mammary epithelial cells during involution.
  • PRL-induced SOCS3 expression in stromal cells is a STAT5a-independent process.

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