CDK1-dependent phosphorylation of EZH2 suppresses methylation of H3K27 and promotes osteogenic differentiation of human mesenchymal stem cells
The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its methyltransferase activity, affecting EZH2-target genes involved in osteogenic differentiation. Enhancer of zeste homologue 2 (EZH2) is the catalytic subuni...
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| Published in | Nature cell biology Vol. 13; no. 1; pp. 87 - 94 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.01.2011
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
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| Abstract | The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its methyltransferase activity, affecting EZH2-target genes involved in osteogenic differentiation.
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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| AbstractList | 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.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. 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. The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its methyltransferase activity, affecting EZH2-target genes involved in osteogenic differentiation. 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. |
| Audience | Academic |
| Author | Chen, Ya-Huey Li, Long-Yuan Yang, Cheng-Chieh Wei, Yongkun Lin, Chun-Yi Hung, Mien-Chie Lai, Chien-Chen Shi, Bin Yeh, Su-Peng Yang, Jer-Yen Lang, Jingyu |
| AuthorAffiliation | 8 Program in Cancer Biology, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA 1 Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA 7 Institute of Molecular Biology, National Chung Hsing University, Taichung 402, Taiwan 2 Center for Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan 3 Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan 6 Graduate Institute of Chinese Medical Science, China Medical University, Taichung 404, Taiwan 4 Asia University, Taichung 413, Taiwan 5 Division of Hematology and Oncology, Department of Medicine, China Medical University and Hospital, Taichung 404, Taiwan |
| AuthorAffiliation_xml | – name: 1 Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030, USA – name: 2 Center for Molecular Medicine, China Medical University Hospital, Taichung 404, Taiwan – name: 3 Graduate Institute of Cancer Biology, China Medical University, Taichung 404, Taiwan – name: 4 Asia University, Taichung 413, Taiwan – name: 6 Graduate Institute of Chinese Medical Science, China Medical University, Taichung 404, Taiwan – name: 8 Program in Cancer Biology, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA – name: 5 Division of Hematology and Oncology, Department of Medicine, China Medical University and Hospital, Taichung 404, Taiwan – name: 7 Institute of Molecular Biology, National Chung Hsing University, Taichung 402, Taiwan |
| Author_xml | – sequence: 1 givenname: Yongkun surname: Wei fullname: Wei, Yongkun organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center – sequence: 2 givenname: Ya-Huey surname: Chen fullname: Chen, Ya-Huey organization: Center for Molecular Medicine, China Medical University Hospital – sequence: 3 givenname: Long-Yuan surname: Li fullname: Li, Long-Yuan email: lyl@mail.cmu.edu.tw organization: Center for Molecular Medicine, China Medical University Hospital, Graduate Institute of Cancer Biology, China Medical University, Asia University – sequence: 4 givenname: Jingyu surname: Lang fullname: Lang, Jingyu organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center – sequence: 5 givenname: Su-Peng surname: Yeh fullname: Yeh, Su-Peng organization: Division of Hematology and Oncology, Department of Medicine, China Medical University and Hospital – sequence: 6 givenname: Bin surname: Shi fullname: Shi, Bin organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center – sequence: 7 givenname: Cheng-Chieh surname: Yang fullname: Yang, Cheng-Chieh organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center – sequence: 8 givenname: Jer-Yen surname: Yang fullname: Yang, Jer-Yen organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center – sequence: 9 givenname: Chun-Yi surname: Lin fullname: Lin, Chun-Yi organization: Center for Molecular Medicine, China Medical University Hospital – sequence: 10 givenname: Chien-Chen surname: Lai fullname: Lai, Chien-Chen organization: Graduate Institute of Chinese Medical Science, China Medical University, Institute of Molecular Biology, National Chung Hsing University – sequence: 11 givenname: Mien-Chie surname: Hung fullname: Hung, Mien-Chie email: mhung@mdanderson.org organization: Department of Molecular and Cellular Oncology, The University of Texas M.D. Anderson Cancer Center, Center for Molecular Medicine, China Medical University Hospital, Graduate Institute of Cancer Biology, China Medical University, Asia University, Program in Cancer Biology, The University of Texas Graduate School of Biomedical Sciences at Houston |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21131960$$D View this record in MEDLINE/PubMed |
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| Snippet | The Polycomb group protein EZH2 promotes trimethylation of histone H3K27 and gene silencing. Cdk1 is found to phosphorylate EZH2 to inhibit its... 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... |
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| SubjectTerms | 2-Aminopurine - analogs & derivatives 2-Aminopurine - pharmacology 631/136/1660 631/80/458/1648 631/80/458/1733 631/80/86 Antibodies Biology Biomedical and Life Sciences Cancer Cancer Research Carrier Proteins - genetics Carrier Proteins - metabolism Catalysis CDC2 Protein Kinase - antagonists & inhibitors CDC2 Protein Kinase - genetics CDC2 Protein Kinase - metabolism Cell Biology Cell Differentiation Cell Line Cell Line, Tumor Cell Movement Cyclin-dependent kinases Developmental Biology DNA-Binding Proteins - genetics DNA-Binding Proteins - metabolism Enhancer of Zeste Homolog 2 Protein Gene expression HEK293 Cells HeLa Cells Histone-Lysine N-Methyltransferase - metabolism Histones - metabolism Humans Immunoblotting Invasiveness Kinases letter Life Sciences Lysine - metabolism Mesenchymal Stem Cells - cytology Mesenchymal Stem Cells - metabolism Methylation Neoplasm Proteins Nuclear Proteins - genetics Nuclear Proteins - metabolism Oncology Osteoblasts - cytology Osteoblasts - metabolism Phosphorylation Physiological aspects Polycomb Repressive Complex 2 Protein Binding Protein kinases Proteins Repressor Proteins - genetics Repressor Proteins - metabolism RNA Interference Stem Cells Threonine - metabolism Transcription Factors - genetics Transcription Factors - metabolism |
| Title | CDK1-dependent phosphorylation of EZH2 suppresses methylation of H3K27 and promotes osteogenic differentiation of human mesenchymal stem cells |
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