Journal article
Sirt3, Mitochondrial ROS, Ageing, and Carcinogenesis
International journal of molecular sciences, Vol.12(9), pp.6226-6239
09/2011
DOI: 10.3390/ijms12096226
PMCID: PMC3189778
PMID: 22016654
Abstract
One fundamental observation in cancer etiology is that the rate of malignancies in any mammalian population increases exponentially as a function of age, suggesting a mechanistic link between the cellular processes governing longevity and carcinogenesis. In addition, it is well established that aberrations in mitochondrial metabolism, as measured by increased reactive oxygen species (ROS), are observed in both aging and cancer. In this regard, genes that impact upon longevity have recently been characterized in
S. cerevisiae
and
C. elegans
, and the human homologs include the Sirtuin family of protein deacetylases. Interestingly, three of the seven sirtuin proteins are localized into the mitochondria suggesting a connection between the mitochondrial sirtuins, the free radical theory of aging, and carcinogenesis. Based on these results it has been hypothesized that Sirt3 functions as a mitochondrial fidelity protein whose function governs both aging and carcinogenesis by modulating ROS metabolism. Sirt3 has also now been identified as a genomically expressed, mitochondrial localized tumor suppressor and this review will outline potential relationships between mitochondrial ROS/superoxide levels, aging, and cell phenotypes permissive for estrogen and progesterone receptor positive breast carcinogenesis.
Details
- Title: Subtitle
- Sirt3, Mitochondrial ROS, Ageing, and Carcinogenesis
- Creators
- Seong-Hoon Park - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsOzkan Ozden - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsHaiyan Jiang - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsYong I Cha - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsJ. Daniel Pennington - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsNukhet Aykin-Burns - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USA; E-MailsDouglas R Spitz - Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USA; E-MailsDavid Gius - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-MailsHyun-Seok Kim - Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA; E-Mails
- Resource Type
- Journal article
- Publication Details
- International journal of molecular sciences, Vol.12(9), pp.6226-6239
- DOI
- 10.3390/ijms12096226
- PMID
- 22016654
- PMCID
- PMC3189778
- NLM abbreviation
- Int J Mol Sci
- ISSN
- 1422-0067
- eISSN
- 1422-0067
- Publisher
- Molecular Diversity Preservation International (MDPI)
- Language
- English
- Date published
- 09/2011
- Academic Unit
- Pathology; Radiation Oncology
- Record Identifier
- 9984047704002771
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