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• Park, S
• Ozden, O
• Jiang, H
• Cha, Y
• Pennington, J
• Aykin-Burns, N
• Spitz, D
• Gius, D
• Kim, H
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• Park, S
• Ozden, O
• Jiang, H
• Cha, Y
• Pennington, J
• Aykin-Burns, N
• Spitz, D
• Gius, D
• Kim, H
• [+] on PubMed
• Park, S
• Ozden, O
• Jiang, H
• Cha, Y
• Pennington, J
• Aykin-Burns, N
• Spitz, D
• Gius, D
• Kim, H

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Int. J. Mol. Sci. 2011, 12(9), 6226-6239; doi:10.3390/ijms12096226

Review

Sirt3, Mitochondrial ROS, Ageing, and Carcinogenesis

Seong-Hoon Park ¹ , Ozkan Ozden ¹ , Haiyan Jiang ¹ , Yong I. Cha ¹ , J. Daniel Pennington ¹ , Nukhet Aykin-Burns ² , Douglas R. Spitz ² , David Gius ¹  and Hyun-Seok Kim ^1,*

¹ Department of Cancer Biology, Pediatrics, and Radiation Oncology, Vanderbilt University Medical Center, Nashville, TN 37232, USA ² Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, IA 52242, USA

* Author to whom correspondence should be addressed.

Received: 21 July 2011; in revised form: 14 September 2011 / Accepted: 20 September 2011 / Published: 23 September 2011

(This article belongs to the Special Issue Oxidative Stress and Mitochondria)

Download PDF Full-Text [303 KB, uploaded 23 September 2011 09:51 CEST]

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.

Keywords: Sirt3; mitochondria; acetylation; acetylome; cancer; MnSOD; carcinogenesis; receptor positive breast cancer

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