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Absence of the steroid receptor coactivator-3 induces B-cell lymphoma

Agnès Coste1, Maria Cristina Antal, Susan Chan

  • 1Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/Université Louis Pasteur, Illkirch, France.

The EMBO Journal
|May 6, 2006
PubMed

Insights

Steroid receptor coactivator 3 (SRC-3) deletion in mice leads to increased lymphocytes and B-cell lymphomas. SRC-3 normally restrains lymphopoiesis by inhibiting NF-kappaB signaling, showing context-dependent roles in cell proliferation.

Area of Science:

  • Molecular Biology
  • Immunology
  • Cancer Research

Background:

  • Steroid receptor coactivator 3 (SRC-3) is a p160 family coactivator crucial for mammary gland development and tumorigenesis.
  • SRC-3's role in other tissues, particularly in lymphopoiesis, is less understood.

Purpose of the Study:

  • To investigate the function of SRC-3 in lymphopoiesis and its impact on lymphoid malignancies.
  • To elucidate the molecular mechanisms by which SRC-3 regulates lymphoid cell proliferation and survival.

Main Methods:

  • Gene deletion studies in mice (SRC-3 knockout).
  • Flow cytometry analysis of lymphocyte populations.
  • Analysis of gene expression related to proliferation and apoptosis.
  • Investigation of NF-kappaB signaling pathway activation.

Main Results:

  • SRC-3 deletion resulted in decreased platelets and increased lymphocytes, leading to B-cell lymphomas in aging mice.
  • Lymphoid lineage expansion was cell-autonomous, linked to induced proliferative/antiapoptotic genes via constitutive NF-kappaB activation.
  • NF-kappaB activation resulted from IkappaB degradation due to increased IkappaB kinase activity, no longer inhibited by SRC-3.
  • Re-expression of SRC-3 reversed the lymphoid expansion.

Conclusions:

  • SRC-3 plays a critical role in regulating lymphopoiesis and preventing lymphoid malignancies.
  • SRC-3 acts as a negative regulator of lymphopoiesis by inhibiting NF-kappaB signaling.
  • SRC-3 exhibits context-dependent effects on cell proliferation, promoting proliferation in breast tissue but inhibiting it in lymphoid cells.

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