SIRT2 is a tumor suppressor that connects aging, acetylome, cell cycle signaling, and carcinogenesis

Seong Hoon Park, Yuming Zhu, Ozkan Ozden, Hyun Seok Kim, Haiyan Jiang, Chu Xia Deng, David Gius, Athanassios Vassilopoulos*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

66 Scopus citations

Abstract

One long standing observation in clinical oncology is that age increase is the single most statistically significant factor/variable that predicts for the incidence of solid tumors. This observation suggests that the cellular and molecular processes and mechanisms that direct an organism's life span may be used to determine the clinical connection between aging and carcinogenesis. In this regard, the genes that impact upon longevity have been characterized in S. cerevisiae and C. elegans, and the human homologs include the Sirtuin family of protein deacetylases. We have recently shown that the primary cytoplasmic sirtuin, Sirt2 appears to meet the criteria as a legitimate tumor suppressor protein. Mice genetically altered to delete Sirt2 develop gender-specific tumorigenesis, with females primarily developing mammary tumors, and males developing multiple different types of gastrointestinal malignancies. Furthermore human tumors, as compared to normal samples, displayed significant decreases in SIRT2 levels suggesting that SIRT2 may also be a human tumor suppressor.

Original languageEnglish (US)
Pages (from-to)15-21
Number of pages7
JournalTranslational Cancer Research
Volume1
Issue number1
DOIs
StatePublished - Jun 1 2012

Keywords

  • APC/C complex
  • Acetylation
  • Cancer
  • Mitosis
  • Sirt2
  • Sirtuins

ASJC Scopus subject areas

  • Oncology
  • Radiology Nuclear Medicine and imaging
  • Cancer Research

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