W
Wen Zhou
Researcher at University of Miami
Publications - 28
Citations - 1442
Wen Zhou is an academic researcher from University of Miami. The author has contributed to research in topics: Acetylation & DNA damage. The author has an hindex of 17, co-authored 28 publications receiving 1309 citations. Previous affiliations of Wen Zhou include University of Padua & Peking University.
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Journal ArticleDOI
Acetylation of p53 at lysine 373/382 by the histone deacetylase inhibitor depsipeptide induces expression of p21(Waf1/Cip1).
Ying Zhao,Shaoli Lu,Lipeng Wu,Guolin Chai,Haiying Wang,Yingqi Chen,Jia Sun,Yu Yu,Wen Zhou,Quanhui Zheng,Mian Wu,Gregory A. Otterson,Wei-Guo Zhu +12 more
TL;DR: It is found that an inhibitor of HDAC, depsipeptide, but not trichostatin A, induces p21Waf1/Cip1 expression through both p53 and Sp1/Sp3 pathways in A549 cells (which retain wild-type p53).
Journal ArticleDOI
Mutant p53 cooperates with the SWI/SNF chromatin remodeling complex to regulate VEGFR2 in breast cancer cells
Neil T. Pfister,Vitalay Fomin,Kausik Regunath,Jeffrey Y. Zhou,Wen Zhou,Laxmi Silwal-Pandit,Laxmi Silwal-Pandit,William A. Freed-Pastor,William A. Freed-Pastor,Oleg Laptenko,Suat Peng Neo,Jill Bargonetti,Mainul Hoque,Bin Tian,Jayantha Gunaratne,Jayantha Gunaratne,Olav Engebraaten,Olav Engebraaten,James L. Manley,Anne Lise Børresen-Dale,Anne Lise Børresen-Dale,Paul M. Neilsen,Carol Prives +22 more
TL;DR: It is surmised that mutant p53 impacts transcription of VEGFR2 as well as myriad other genes by promoter remodeling through interaction with and likely regulation of the SWI/SNF chromatin remodeling complex, which means that not only might mutants p53-expressing tumors be susceptible to anti VEGF therapies, impacting SWI-SNF tumor suppressor function in mutant p 53 tumors may also have therapeutic potential.
Journal ArticleDOI
Links between oestrogen receptor activation and proteolysis: relevance to hormone-regulated cancer therapy
Wen Zhou,Joyce M. Slingerland +1 more
TL;DR: The elucidation of mechanisms whereby oestrogen drives both ERα transactivation and receptor proteolysis might have important therapeutic implications not only for breast cancer but also potentially for other hormone-regulated cancers.
Journal ArticleDOI
Histone Deacetylase Inhibitor Depsipeptide Activates Silenced Genes through Decreasing both CpG and H3K9 Methylation on the Promoter
Lipeng Wu,Xi Wang,Lian Li,Ying Zhao,Shaoli Lu,Yu Yu,Wen Zhou,Xiangyu Liu,Jing Yang,Zhixin Zheng,Hui Zhang,Jingnan Feng,Yang Yang,Haiying Wang,Wei-Guo Zhu +14 more
TL;DR: A novel mechanism of HDACi-mediated DNA demethylation via suppression of histone methyltransferases and reduced recruitment of HP1 and DNMT1 to the genes' promoter is described.
Journal ArticleDOI
Acetylation of FoxO1 Activates Bim Expression to Induce Apoptosis in Response to Histone Deacetylase Inhibitor Depsipeptide Treatment
Yang Yang,Ying Zhao,Wenjuan Liao,Jing Yang,Lipeng Wu,Zhixing Zheng,Yu Yu,Wen Zhou,Lian Li,Jingnan Feng,Haiying Wang,Wei-Guo Zhu +11 more
TL;DR: In this article, the authors showed that depsipeptide-induced expression of Bim was directly dependent on acetylation of forkhead box class O1 (FoxO1) that is catalyzed by cyclic adenosine monophosphate-responsive element-binding protein-binding proteins, and indirectly induced by a decreased four-and-a-half LIM-domain protein 2.