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c-myc as a mediator of accelerated apoptosis and involution in mammary glands lacking Socs3

Kate D Sutherland1, François Vaillant, Warren S Alexander

  • 1VBCRC Laboratory, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.

The EMBO Journal
|December 2, 2006
PubMed

Insights

Suppressor of cytokine signalling 3 (Socs3) is not vital for normal mammary gland function during pregnancy. However, its absence accelerates mammary gland involution by increasing apoptosis and c-myc levels.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Molecular Biology

Background:

  • Suppressor of cytokine signalling (SOCS) proteins regulate cytokine signalling pathways.
  • SOCS proteins are crucial for maintaining tissue homeostasis and preventing aberrant signalling.
  • The role of SOCS family members, particularly SOCS3, in mammary gland development requires further elucidation.

Purpose of the Study:

  • To investigate the specific role of SOCS3 in mammary epithelial cell function during mammary gland development.
  • To determine if SOCS3 is essential for prolactin signalling and mammary gland maintenance.
  • To elucidate the molecular mechanisms underlying mammary gland involution in the absence of SOCS3.

Main Methods:

  • Generation of mice with mammary epithelial cell-specific deletion of Socs3.
  • Analysis of mammary gland phenotypes during pregnancy, lactation, and involution.
  • Assessment of epithelial apoptosis, tissue remodelling, and key signalling pathway activation (e.g., Stat3).
  • Investigation of c-myc expression and its downstream targets in Socs3-deficient mammary glands.

Main Results:

  • Mammary glands lacking Socs3 showed no overt phenotype during pregnancy and lactation, suggesting Socs3 is not critical for prolactin signalling.
  • Socs3-deficient mammary glands exhibited increased epithelial apoptosis and tissue remodelling, leading to premature involution.
  • This phenotype was associated with enhanced Stat3 activation and elevated c-myc levels.
  • Induction of c-myc mimicked the Socs3-deficient phenotype, with increased expression of apoptosis-related genes (E2F-1, Bax, p53).

Conclusions:

  • SOCS3 acts as a critical regulator, attenuating pro-apoptotic pathways in the developing mammary gland.
  • The study provides evidence that c-myc plays a significant role in regulating apoptosis during mammary gland involution.
  • These findings highlight SOCS3's importance in maintaining mammary gland integrity and preventing precocious involution.

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