The Arf/p53 protein module, which induces apoptosis, down-regulates histone H2AX to allow normal cells to survive in the presence of anti-cancer drugs

Abstract

Background: It is unclear how DNA-damaging agents target cancer cells over normal somatic cells. Results: Arf/p53-dependent down-regulation of H2AX enables normal cells to survive after DNA damage. Conclusion: Transformed cells, which harbor mutations in either Arf or p53, are more sensitive to DNA-damaging agents. Significance: Cellular transformation renders cells more susceptible to some DNA-damaging agents. Copyright © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.