SIRT2 as a new player in epigenetic programming of keratinocyte differentiation and a candidate tumor suppressor

Ming Wang, Zhicao Yue, Ralf Paus, Yuval Ramot

Research output: Contribution to journalComment/debate

8 Scopus citations

Abstract

Epidermal keratinocytes undergo a continuous process of terminal differentiation, which is accompanied by a dramatic change in the expression and composition of keratins. This complex and carefully orchestrated process is regulated by a large number of signal transduction events and transcriptional factors as well as by epigenetic regulatory mechanisms, namely by histone methylation/acetylation and DNA methylation. In a recent issue of Exp Dermatol, Ming et al. provide evidence that sirtuin-2 (SIRT2), a NAD+-dependent deacetylase, inhibits the expression of keratin 15 and keratin 19, epidermal stem cell markers, while it stimulates the expression of loricrin, a marker of terminal keratinocyte differentiation. Human skin cancer cells show downregulation of SIRT2, and its deletion increases tumor growth in mice. Overall, these findings suggest that this deacetylase is involved in the epigenetic regulation of keratinocyte differentiation and exerts intracutaneous tumor suppressor functions.

Original languageEnglish (US)
Pages (from-to)636-638
Number of pages3
JournalExperimental Dermatology
Volume23
Issue number9
DOIs
StatePublished - Jan 1 2014
Externally publishedYes

Keywords

  • Epigenetic programming
  • Keratinocyte differentiation
  • SIRT2

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

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