Journal
NATURE CELL BIOLOGY
Volume 13, Issue 1, Pages 87-U211Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2139
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Funding
- National Institutes of Health [R01 CA109311]
- Kadoorie Charitable Foundations
- National Breast Cancer Foundation Inc.
- M.D. Anderson Cancer Center/China Medical University and Hospital
- [NSC 96-3111-B-039]
- [NSC 97-3111-B-039]
- [NHRI-EX98-9603BC]
- [DOH97-TD-I-111-TM003]
- [DOH98-TD-I-111-TM002]
- [DOH97-TD-G-111-041]
- [DOH99-TD-C-111-005]
- [NSC99-2632-B-039-001-MY3]
- NATIONAL CANCER INSTITUTE [R01CA109311, P01CA099031] Funding Source: NIH RePORTER
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Enhancer of zeste homologue 2 (EZH2) is the catalytic subunit of Polycomb repressive complex 2 (PRC2) and catalyses the trimethylation of histone H3 on Lys 27 (H3K27), which represses gene transcription. EZH2 enhances cancer-cell invasiveness and regulates stem cell differentiation. Here, we demonstrate that EZH2 can be phosphorylated at Thr 487 through activation of cyclin-dependent kinase 1 (CDK1). The phosphorylation of EZH2 at Thr 487 disrupted EZH2 binding with the other PRC2 components SUZ12 and EED, and thereby inhibited EZH2 methyltransferase activity, resulting in inhibition of cancer-cell invasion. In human mesenchymal stem cells, activation of CDK1 promoted mesenchymal stem cell differentiation into osteoblasts through phosphorylation of EZH2 at Thr 487. These findings define a signalling link between CDK1 and EZH2 that may have an important role in diverse biological processes, including cancer-cell invasion and osteogenic differentiation of mesenchymal stem cells.
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