p53 and MDM2: antagonists or partners in crime?

Christine M Eischen; Guillermina Lozano

doi:10.1016/j.ccr.2009.02.004

p53 and MDM2: antagonists or partners in crime?

Cancer Cell. 2009 Mar 3;15(3):161-2. doi: 10.1016/j.ccr.2009.02.004.

Authors

Christine M Eischen¹, Guillermina Lozano

Affiliation

¹ Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.

PMID: 19249672
DOI: 10.1016/j.ccr.2009.02.004

Abstract

Therapeutics that disrupt the p53-MDM2 interaction show promise for cancer treatment but surprisingly have different biological outcomes. A study by Enge et al. in this issue of Cancer Cell shows that the ability of MDM2 to target hnRNP K for degradation contributes to the decision to induce apoptosis rather than cell-cycle arrest.

Publication types

Review
Comment

MeSH terms

Animals
Antineoplastic Agents / pharmacology
Apoptosis / physiology*
Cell Cycle / drug effects
Gene Expression Regulation
Humans
Neoplasms / drug therapy
Neoplasms / metabolism
Proto-Oncogene Proteins c-mdm2 / metabolism*
Tumor Suppressor Protein p53 / metabolism*

Substances

Antineoplastic Agents
Tumor Suppressor Protein p53
Proto-Oncogene Proteins c-mdm2