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

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.

journal_name

Exp Dermatol

journal_title

Experimental dermatology

authors

Wang M,Yue Z,Paus R,Ramot Y

doi

10.1111/exd.12434

subject

Has Abstract

pub_date

2014-09-01 00:00:00

pages

636-8

issue

9

eissn

0906-6705

issn

1600-0625

journal_volume

23

pub_type

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