Title of article
SIRT3 Is a Mitochondria-Localized Tumor Suppressor Required for Maintenance of Mitochondrial Integrity and Metabolism during Stress
Author/Authors
Kim، نويسنده , , Hyun-Seok and Patel، نويسنده , , Krish and Muldoon-Jacobs، نويسنده , , Kristi and Bisht، نويسنده , , Kheem S. and Aykin-Burns، نويسنده , , Nukhet and Pennington، نويسنده , , J. Daniel and van der Meer، نويسنده , , Riet and Nguyen، نويسنده , , Phuongmai and Savage، نويسنده , , Jason and Owens، نويسنده , , Kjerstin M. and Vassilopoulos، نويسنده , , Athanassios and Ozden، نويسنده , , Ozkan and Park، نويسنده , , Seong-Hoon and Singh، نويسنده , , Keshav K. and Abdulkadir، نويسنده , , Sarki A. and Spitz، نويسنده , , Douglas R. and Deng، نويسنده , , Chu-Xia and Gius، نويسنده , , David، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2010
Pages
12
From page
41
To page
52
Abstract
Summary
rtuin gene family (SIRT) is hypothesized to regulate the aging process and play a role in cellular repair. This work demonstrates that SIRT3−/− mouse embryonic fibroblasts (MEFs) exhibit abnormal mitochondrial physiology as well as increases in stress-induced superoxide levels and genomic instability. Expression of a single oncogene (Myc or Ras) in SIRT3−/− MEFs results in in vitro transformation and altered intracellular metabolism. Superoxide dismutase prevents transformation by a single oncogene in SIRT3−/− MEFs and reverses the tumor-permissive phenotype as well as stress-induced genomic instability. In addition, SIRT3−/− mice develop ER/PR-positive mammary tumors. Finally, human breast and other human cancer specimens exhibit reduced SIRT3 levels. These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor.
Keywords
CELLCYCLE , Proteins
Journal title
Cancer Cell
Serial Year
2010
Journal title
Cancer Cell
Record number
1337017
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