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PMID: 20303758 Published · ppublish English Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Review

p53 and ARF: unexpected players in autophagy.

Trends in cell biology ·Vol. 20 ·No. 6 ·2010-06-00 ·Pages 363-9

Balaburski GM, Hontz RD, Murphy ME

Abstract

p53 and ARF are well-established tumor-suppressor proteins that function together in the negative regulation of cancer. Recently, both proteins were found to play surprising roles in autophagy. Autophagy ('self-eating') is a crucial response of eukaryotic cells to metabolic and other stress. During this process, portions of the cytosol are sequestered into characteristic double-membrane vesicles that are delivered to the lysosome for degradation, leading to the release of free amino acids and promoting cell survival. The mechanisms whereby p53 and ARF control autophagy are only now becoming elucidated. An emerging question is whether we can develop metabolic poisons that preferentially destroy tumor cells depending on their reliance on autophagy for survival, and on their p53 and ARF status.

MeSH Terms
Animals Autophagy Cyclin-Dependent Kinase Inhibitor p16/metabolism Humans Tumor Suppressor Protein p14ARF/metabolism Tumor Suppressor Protein p53/metabolism
Chemicals
Cyclin-Dependent Kinase Inhibitor p16 Tumor Suppressor Protein p14ARF Tumor Suppressor Protein p53
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Balaburski Gregor M
Program in Molecular and Translational Medicine, Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA.
Hontz Robert D
Murphy Maureen E
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Article Info
Journal
Trends in cell biology
Abbr.
Trends Cell Biol
ISSN
1879-3088
Published
2010-06-00
Epub
2010-00-19
Pages
363-9
Language
English
Region
England
NLM ID
9200566
PMCID
PMC2891045
Subset
IM
Grants
NCI NIH HHS · R01 CA102184 · United States
NCI NIH HHS · R01 CA102184-05A1 · United States
NCI NIH HHS · R01 CA139319 · United States
NCI NIH HHS · R01 CA139319-01A1 · United States
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