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Association of the cyclin-dependent kinases and 14-3-3 sigma negatively regulates cell cycle progression

C Laronga1, H Y Yang, C Neal

  • 1Departments of Surgical Oncology/Molecular and Cellular Oncology and the Breast Cancer Research Program, the University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, USA.

The Journal of Biological Chemistry
|April 18, 2000
PubMed

Insights

14-3-3 sigma protein, a cell cycle regulator, was identified through its association with cyclin-dependent kinase 2 (CDK2). Its overexpression inhibits cell cycle progression and proliferation, suggesting a role in preventing breast tumor growth.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • 14-3-3 sigma is involved in p53-mediated cell cycle arrest.
  • It shares binding motifs with known cell cycle regulators.

Purpose of the Study:

  • To clone 14-3-3 sigma using expression cloning.
  • To investigate its role in cell cycle regulation and breast cancer.

Main Methods:

  • Expression cloning based on cyclin-dependent kinase 2 (CDK2) association.
  • In vitro and in vivo association studies with cyclin-CDK complexes.
  • Overexpression studies in breast cancer cell lines.

Main Results:

  • 14-3-3 sigma was cloned via CDK2 association.
  • It associates with cyclin-CDK complexes.
  • Overexpression inhibits cyclin-CDK activity, cell cycle entry, proliferation, and anchorage-independent growth in breast cancer cells.

Conclusions:

  • 14-3-3 sigma acts as a negative regulator of cell cycle progression.
  • It plays a significant role in inhibiting breast tumor cell growth.

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