YY1 restrained cell senescence through repressing the transcription of p16.

Xiuli Wang; Yunpeng Feng; Liang Xu; Yuli Chen; Yu Zhang; Dongmei Su; Guoling Ren; Jun Lu; Baiqu Huang

doi:10.1016/j.bbamcr.2008.05.015

YY1 restrained cell senescence through repressing the transcription of p16.

Xiuli Wang, Yunpeng Feng, Liang Xu, Yuli Chen, Yu Zhang, Dongmei Su, Guoling Ren, Jun Lu, Baiqu Huang

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

45 Citationer (Scopus)

Abstract

Udgivelsesdato: 2008-Oct

Originalsprog	Engelsk
Tidsskrift	BBA General Subjects
Vol/bind	1783
Udgave nummer	10
Sider (fra-til)	1876-83
Antal sider	7
ISSN	0304-4165
DOI	https://doi.org/10.1016/j.bbamcr.2008.05.015
Status	Udgivet - 2008
Udgivet eksternt	Ja

Adgang til dokumentet

10.1016/j.bbamcr.2008.05.015

Citationsformater

@article{dc095f90a73511ddb5e9000ea68e967b,

title = "YY1 restrained cell senescence through repressing the transcription of p16.",

abstract = "The transcription factor YY1 has been implicated to play a role in cell growth control. In this report, we demonstrate that YY1 was able to suppress NCI-H460 cell senescence through regulating the expression of p16(INK4a), a cyclin-dependent kinase inhibitor. We also show that YY1 participated in the repression of p16(INK4a) expression in 293T cells through an epigenetic mechanism involving histone acetylation modification. Specifically, HDAC3 and HDAC4 inhibited the p16(INK4a) promoter activity. The chromatin immunoprecipitation (ChIP) assays verified that HDAC3 and HDAC4 were recruited to p16(INK4a) promoter by YY1. Moreover, co-immunoprecipitation assays revealed that these three protein factors formed a complex. Furthermore, knockdown of these factors induced cell enlargement and flattened morphology and significantly increased the SA-beta-gal activity, a biochemical marker of cell senescence. Overall, data from this study suggest that YY1, HDAC3 and HDAC4 restrained cell senescence by repressing p16(INK4a) expression through an epigenetic modification of histones.",

author = "Xiuli Wang and Yunpeng Feng and Liang Xu and Yuli Chen and Yu Zhang and Dongmei Su and Guoling Ren and Jun Lu and Baiqu Huang",

year = "2008",

doi = "10.1016/j.bbamcr.2008.05.015",

language = "English",

volume = "1783",

pages = "1876--83",

journal = "BBA General Subjects",

issn = "0304-4165",

publisher = "Elsevier",

number = "10",

}

TY - JOUR

T1 - YY1 restrained cell senescence through repressing the transcription of p16.

AU - Wang, Xiuli

AU - Feng, Yunpeng

AU - Xu, Liang

AU - Chen, Yuli

AU - Zhang, Yu

AU - Su, Dongmei

AU - Ren, Guoling

AU - Lu, Jun

AU - Huang, Baiqu

PY - 2008

Y1 - 2008

N2 - The transcription factor YY1 has been implicated to play a role in cell growth control. In this report, we demonstrate that YY1 was able to suppress NCI-H460 cell senescence through regulating the expression of p16(INK4a), a cyclin-dependent kinase inhibitor. We also show that YY1 participated in the repression of p16(INK4a) expression in 293T cells through an epigenetic mechanism involving histone acetylation modification. Specifically, HDAC3 and HDAC4 inhibited the p16(INK4a) promoter activity. The chromatin immunoprecipitation (ChIP) assays verified that HDAC3 and HDAC4 were recruited to p16(INK4a) promoter by YY1. Moreover, co-immunoprecipitation assays revealed that these three protein factors formed a complex. Furthermore, knockdown of these factors induced cell enlargement and flattened morphology and significantly increased the SA-beta-gal activity, a biochemical marker of cell senescence. Overall, data from this study suggest that YY1, HDAC3 and HDAC4 restrained cell senescence by repressing p16(INK4a) expression through an epigenetic modification of histones.

AB - The transcription factor YY1 has been implicated to play a role in cell growth control. In this report, we demonstrate that YY1 was able to suppress NCI-H460 cell senescence through regulating the expression of p16(INK4a), a cyclin-dependent kinase inhibitor. We also show that YY1 participated in the repression of p16(INK4a) expression in 293T cells through an epigenetic mechanism involving histone acetylation modification. Specifically, HDAC3 and HDAC4 inhibited the p16(INK4a) promoter activity. The chromatin immunoprecipitation (ChIP) assays verified that HDAC3 and HDAC4 were recruited to p16(INK4a) promoter by YY1. Moreover, co-immunoprecipitation assays revealed that these three protein factors formed a complex. Furthermore, knockdown of these factors induced cell enlargement and flattened morphology and significantly increased the SA-beta-gal activity, a biochemical marker of cell senescence. Overall, data from this study suggest that YY1, HDAC3 and HDAC4 restrained cell senescence by repressing p16(INK4a) expression through an epigenetic modification of histones.

U2 - 10.1016/j.bbamcr.2008.05.015

DO - 10.1016/j.bbamcr.2008.05.015

M3 - Journal article

C2 - 18558095

SN - 0304-4165

VL - 1783

SP - 1876

EP - 1883

JO - BBA General Subjects

JF - BBA General Subjects

IS - 10

ER -