期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 108, 期 33, 页码 13379-13386出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1110104108
关键词
mouse model; histone methyltransferase; chromatin modifier; neuroendocrine tumor; islet cell tumor
资金
- National Institutes of Health [CA138631, CA076120, CA16359]
- Raymond and Beverly Sackler Fund for the Arts and Sciences
- Caring for Carcinoid Foundation
- V Scholar Award
- Grants-in-Aid for Scientific Research [23659175, 23310136] Funding Source: KAKEN
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.
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