Oncogenic H-ras induces cyclin B1 expression in a p53-independent manner

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Updated: Sep 28, 2026

Analysis of Cell Cycle Position in Mammalian Cells
12:19

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Carla Santana1, Enrique Ortega, Alejandro García-Carrancá

  • 1Department of Molecular Biology and Biotechnology, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico.

Mutation Research
|October 16, 2002
PubMed

Insights

The H-ras oncogene regulates cyclin B1 expression and G2/M checkpoint control independently of p53. This suggests H-ras influences cell cycle progression through novel p53-independent pathways.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • The p53 tumor suppressor is crucial for G2 checkpoint control, often by repressing cyclin B1 transcription.
  • Emerging evidence highlights p53-independent mechanisms regulating cell cycle progression.
  • Ras proteins are implicated in controlling both G1/S and G2/M transitions.

Purpose of the Study:

  • To investigate whether the H-ras oncogene can regulate cyclin B1 expression in a p53-independent manner.
  • To elucidate the role of H-ras in G2/M checkpoint control independent of p53 function.

Main Methods:

  • Assessed cyclin B1 promoter activity in SW480 cells with null p53 alleles upon H-ras oncogene expression.
  • Examined cyclin B1 mRNA and protein levels in HeLa cells (expressing HPV18 E6 to inactivate p53) transfected with H-ras.
  • Measured cyclin B1/cdc2 complex levels and kinase activity.
  • Evaluated G2/M checkpoint response to DNA damage.

Main Results:

  • H-ras oncogene induced cyclin B1 promoter activity in p53-null SW480 cells.
  • Transfection with H-ras increased cyclin B1 mRNA and protein in p53-inactivated HeLa cells.
  • Elevated cyclin B1 expression correlated with increased cyclin B1/cdc2 complex and kinase activity.
  • The cyclin B1/cdc2 complex showed no inhibition at G2/M following DNA damage.

Conclusions:

  • H-ras oncogene plays a role in regulating cyclin B1 expression through p53-independent pathways.
  • H-ras influences G2/M checkpoint control via modulation of cyclin B1, independent of p53 status.
  • These findings reveal a novel mechanism for cell cycle regulation by H-ras in the context of compromised p53 function.

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