title: p53 and MDM2: antagonists or partners in crime?
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.
authors.affiliation: Department of Pathology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
authors.forename: Christine M
authors.initials: CM
authors.lastname: Eischen
authors.forename: Guillermina
authors.initials: G
authors.lastname: Lozano
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000502:physiology*; D002453:Cell Cycle / Q000187:drug effects; D005786:Gene Expression Regulation; D006801:Humans; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism; D051736:Proto-Oncogene Proteins c-mdm2 / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D016159:Tumor Suppressor Protein p53; D051736:Proto-Oncogene Proteins c-mdm2