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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Control of cyclin D1 and breast tumorigenesis by the EglN2 prolyl hydroxylase

Qing Zhang1, Jinming Gu, Lianjie Li

  • 1Department of Medical Oncology, Dana-Farber Cancer Institute and Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Cancer Cell
|November 3, 2009
PubMed

Insights

EglN2 inactivation suppresses estrogen-driven breast cancer by reducing Cyclin D1 levels. This discovery highlights EglN2 as a potential therapeutic target for breast cancer and other malignancies.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • 2-Oxoglutarate-dependent dioxygenases, such as EglN prolyl hydroxylases, regulate Hypoxia-Inducible Factor (HIF) and are targets for drug development.
  • EglN2 is estrogen-inducible in breast carcinoma cells and interacts with Cyclin D1 in Drosophila.

Purpose of the Study:

  • To investigate the role of EglN2 in estrogen-dependent breast cancer.
  • To determine if EglN2 inhibition can suppress tumor growth.

Main Methods:

  • Gene inactivation of EglN2 in vivo.
  • Analysis of Cyclin D1 levels and mammary gland proliferation.
  • Assessment of estrogen-dependent breast cancer tumorigenesis.
  • Evaluation of EglN2 depletion in various cancer cell lines.

Main Results:

  • EglN2 inactivation decreased Cyclin D1 levels and suppressed mammary gland proliferation.
  • EglN2's regulation of Cyclin D1 is specific and HIF-independent.
  • Loss of EglN2 catalytic activity inhibited estrogen-dependent breast cancer growth, which was rescued by exogenous Cyclin D1.
  • EglN2 depletion impaired the fitness of lung, brain, and hematopoietic cancer lines.

Conclusions:

  • EglN2 plays a critical role in estrogen-dependent breast cancer proliferation and tumorigenesis.
  • EglN2 is a potential therapeutic target for estrogen-dependent breast cancer and other cancers.

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