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The steroid receptor coactivator-3 is a tumor promoter in a mouse model of thyroid cancer

H Ying1, M C Willingham, S-Y Cheng

  • 1Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4264, USA.

Oncogene
|July 27, 2007
PubMed

Insights

Steroid receptor coactivator-3 (SRC-3) significantly impacts thyroid cancer development. Its deficiency in mice reduced tumor growth, slowed progression, and decreased metastasis, offering potential therapeutic insights.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Thyroid carcinogenesis molecular events remain unclear.
  • Thyroid hormone receptor-beta (TRbeta) mutations drive follicular thyroid carcinoma in mice.
  • Steroid receptor coactivator-3 (SRC-3) role in thyroid cancer is unknown.

Purpose of the Study:

  • Investigate SRC-3's role in thyroid carcinogenesis in vivo.
  • Utilize TRbeta(PV/PV) and SRC-3(-/-) mouse models.

Main Methods:

  • Crossed TRbeta(PV/PV) and SRC-3(-/-) mice.
  • Analyzed survival, tumor growth, progression, and metastasis.
  • Performed in vivo and in vitro signaling pathway analyses.

Main Results:

  • SRC-3 deficiency (TRbeta(PV/PV)SRC-3(-/-)) increased survival and reduced tumor growth compared to SRC-3-positive mice (TRbeta(PV/PV)SRC-3(+/+)).
  • SRC-3 deficiency inhibited cell cycle progression (G1/S transition) via E2F1.
  • SRC-3 deficiency induced apoptosis (Bcl-2, caspase-3) and suppressed neovascularization/metastasis (VEGF).

Conclusions:

  • SRC-3 plays a critical role in thyroid carcinogenesis.
  • SRC-3 regulates multiple genes and signaling pathways.
  • Understanding SRC-3's function may guide future thyroid cancer therapeutics.

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