Format

Send to

Choose Destination
Curr Opin Oncol. 2014 Jan;26(1):78-85. doi: 10.1097/CCO.0000000000000024.

To be, or not to be: functional dilemma of p53 metabolic regulation.

Author information

1
Institute for Cancer Genetics, and Department of Pathology and Cell Biology, College of Physicians & Surgeons, Columbia University, New York, USA.

Abstract

PURPOSE OF REVIEW:

In recent years, the emerging role of p53 in metabolic regulation has been a topic of great interest. Although apoptotic and growth arrest functions of p53 remain as important mechanisms for preserving genomic stability, metabolic functions of p53 show increasing potential in contributing to p53-mediated tumor suppression. Numerous recent studies provided further insights into the metabolic functions of p53 and their implications in tumorigenesis.

RECENT FINDINGS:

Several novel p53 metabolic targets have been identified that participate in various aspects of metabolism. Although some studies demonstrate the potential tumor suppressive function of p53 metabolic genes, others reveal prosurvival roles of those targets in both tumor and normal cells. Specifically, Tp53-induced glycolysis and apoptosis regulator (TIGAR) has been thought to promote tumor suppression through metabolic fine-tuning, yet, TIGAR-deficient mice display reduction in tumorigenesis. Finally, characterization of the 3KR mouse model underscored the significance of p53 metabolic regulation in tumor suppression, while also alluding to the potential mechanism for selective regulation of p53 metabolic targets.

SUMMARY:

Expression of many p53 metabolic genes elicits both antitumor and tumorigenic effects, suggesting that p53 may contribute to cellular protection as well as tumor suppression. Future studies must carefully dissect the duality of p53 metabolic function, which may potentially prove useful in designing cancer therapies.

PMID:
24240177
PMCID:
PMC3968813
DOI:
10.1097/CCO.0000000000000024
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wolters Kluwer Icon for PubMed Central
Loading ...
Support Center