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14-3-3sigma is a p53-regulated inhibitor of G2/M progression

H Hermeking1, C Lengauer, K Polyak

  • 1Johns Hopkins Oncology Center, Baltimore, Maryland, USA.

Molecular Cell
|July 11, 1998
PubMed

Insights

Ionizing radiation triggers G2 cell-cycle arrest in colorectal cancer cells via p53-induced 14-3-3sigma. This conserved mechanism highlights 14-3-3sigma

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Cycle Regulation

Background:

  • Colorectal cancer (CRC) cells exhibit G1 and G2 cell-cycle arrest after ionizing radiation exposure.
  • The G1 arrest mechanism involves p53-mediated p21WAF1/CIP1/SDI1 induction.
  • The molecular basis for G2 arrest in CRC cells remained largely unknown.

Purpose of the Study:

  • To elucidate the molecular mechanism underlying G2 cell-cycle arrest in colorectal cancer cells following DNA damage.
  • To identify key genes and pathways involved in radiation-induced G2 arrest.

Main Methods:

  • Quantitative gene expression analysis in CRC cell lines.
  • Investigation of p53-responsive elements and gene induction.
  • Functional studies involving exogenous introduction of identified genes.

Main Results:

  • 14-3-3sigma expression is significantly induced by gamma irradiation and DNA-damaging agents in CRC cells.
  • p53-responsive element located upstream of the 14-3-3sigma gene mediates its induction.
  • Introduction of 14-3-3sigma into cells causes G2 cell-cycle arrest.

Conclusions:

  • 14-3-3sigma is a critical mediator of p53-regulated G2/M cell-cycle arrest in human colorectal cancer cells.
  • The identified G2 arrest mechanism involving 14-3-3sigma is conserved across eukaryotic evolution.
  • This finding provides a molecular target for understanding and potentially manipulating cancer cell response to radiation therapy.

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