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

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...

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Bibliographic Details
Published in:Experimental dermatology 2014-09, Vol.23 (9), p.636-638
Main Authors: Wang, Ming, Yue, Zhicao, Paus, Ralf, Ramot, Yuval
Format: Article
Language:English
Subjects:
Animals
Carcinogenesis - chemically induced
Carcinoma, Squamous Cell - genetics
epigenetic programming
Humans
Keratin-19 - genetics
keratinocyte differentiation
SIRT2
Sirtuin 2 - genetics
Sirtuin 2 - metabolism
Skin Neoplasms - genetics
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Summary: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.
ISSN:0906-6705
1600-0625
DOI:10.1111/exd.12434