| Literature DB >> 21788502 |
Wenchu Lin1, Jian Cao, Jiayun Liu, Michael L Beshiri, Yuko Fujiwara, Joshua Francis, Andrew D Cherniack, Christoph Geisen, Lauren P Blair, Mike R Zou, Xiaohua Shen, Dan Kawamori, Zongzhi Liu, Chiara Grisanzio, Hideo Watanabe, Yoji Andrew Minamishima, Qing Zhang, Rohit N Kulkarni, Sabina Signoretti, Scott J Rodig, Roderick T Bronson, Stuart H Orkin, David P Tuck, Elizaveta V Benevolenskaya, Matthew Meyerson, William G Kaelin, Qin Yan.
Abstract
Aberrations in epigenetic processes, such as histone methylation, can cause cancer. Retinoblastoma binding protein 2 (RBP2; also called JARID1A or KDM5A) can demethylate tri- and dimethylated lysine 4 in histone H3, which are epigenetic marks for transcriptionally active chromatin, whereas the multiple endocrine neoplasia type 1 (MEN1) tumor suppressor promotes H3K4 methylation. Previous studies suggested that inhibition of RBP2 contributed to tumor suppression by the retinoblastoma protein (pRB). Here, we show that genetic ablation of Rbp2 decreases tumor formation and prolongs survival in Rb1(+/-) mice and Men1-defective mice. These studies link RBP2 histone demethylase activity to tumorigenesis and nominate RBP2 as a potential target for cancer therapy.Entities:
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Year: 2011 PMID： 21788502 PMCID： PMC3158206 DOI： 10.1073/pnas.1110104108
Source DB: PubMed Journal: Proc Natl Acad Sci U S A ISSN： 0027-8424 Impact factor: 11.205