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Updated: Sep 21, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

[Changes in the activity of cyclin-kinase complexes governing cell transition from G1 phase to DNA replication phase

A M Neliudova1, N D Aksenov, T V Pospelova

  • 1Institute of Cytology RAS, St. Petersburg.

Tsitologiia
|May 2, 2003
PubMed

Insights

The human bcl-2 gene inhibits proliferation in transformed rat cells, inducing G1/S arrest via cyclin E-cdk2 activity changes after irradiation or serum starvation. Adriamycin triggers arrest independently of cyclin-cdk activity.

Area of Science:

  • Cell biology
  • Molecular oncology
  • Cancer research

Context:

  • Transformed rat embryo fibroblasts (E1A + c-Ha-ras) exhibit checkpoint deficiencies and high apoptosis sensitivity.
  • The role of Bcl-2 in regulating cell cycle progression in such cells is not fully understood.

Purpose:

  • To investigate the antiproliferative effects of the human bcl-2 gene in E1A + c-Ha-ras-transformed rat embryo fibroblasts.
  • To elucidate the mechanisms underlying bcl-2-mediated cell cycle arrest induced by various damaging agents.

Summary:

  • Bcl-2 gene transfer induced G1/S arrest in transformed fibroblasts, independent of cyclin E and A protein levels.
  • Irradiation and serum starvation led to G1/S arrest with decreased cyclin E-cdk2 activity, while adriamycin treatment induced arrest independent of cyclin-cdk activity.
  • Bcl-2 overexpression elevated p21/Waf-1 but did not restore inhibitor function, suggesting damage-specific pathways regulate cell cycle arrest.

Impact:

  • Bcl-2 influences cell cycle arrest pathways differently depending on the inducing agent.
  • Findings suggest distinct mechanisms for G1/S arrest, involving either cyclin-cdk activity modulation or downstream targets.
  • Provides insights into bcl-2's role in cancer development and potential therapeutic strategies targeting cell cycle regulation.

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