G1 cyclins link proliferation, pluripotency and differentiation of embryonic stem cells

Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the ab...

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Published inNature cell biology Vol. 19; no. 3; pp. 177 - 188
Main Authors Liu, Lijun, Michowski, Wojciech, Inuzuka, Hiroyuki, Shimizu, Kouhei, Nihira, Naoe Taira, Chick, Joel M., Li, Na, Geng, Yan, Meng, Alice Y., Ordureau, Alban, Kołodziejczyk, Aleksandra, Ligon, Keith L., Bronson, Roderick T., Polyak, Kornelia, Harper, J. Wade, Gygi, Steven P., Wei, Wenyi, Sicinski, Piotr
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.03.2017
Nature Publishing Group
Subjects
13/1
13/100
13/106
13/2
13/31
13/44
13/51
45/23
45/88
45/91
631/532
631/532/2064/1519
631/80/641
631/80/83
Analysis
Animals
Biology
Biomarkers - metabolism
Cancer
Cancer Research
Cell Biology
Cell Cycle
Cell Differentiation
Cell growth
Cell Proliferation
Cell Separation
Cyclin G1 - metabolism
Cyclin-dependent kinases
Cyclins
Developmental Biology
DNA - analysis
Embryo, Mammalian - cytology
Embryonic stem cells
Epigenesis, Genetic
Experiments
Female
Flow Cytometry
Gene Expression Profiling
Genetic aspects
Growth
Histones - metabolism
Hormones - pharmacology
Imaging, Three-Dimensional
Kinases
Life Sciences
Lysine - metabolism
Mammary Glands, Animal - cytology
Mammary Glands, Animal - embryology
Methylation
Mice
Mice, Inbred C57BL
Mouse Embryonic Stem Cells - cytology
Mouse Embryonic Stem Cells - metabolism
Pathology
Properties
Proteins
Receptors, G-Protein-Coupled - metabolism
RNA - analysis
Stem Cells
Steroids - pharmacology
Tetraspanins - metabolism
United States > US
Massachusetts
Online AccessGet full text
ISSN1465-7392
1476-4679
1476-4679
DOI10.1038/ncb3474

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Abstract Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential. Liu et al.  show that G1 cyclins and their cyclin-dependent kinases regulate the pluripotent state by driving phosphorylation of Nanog, Oct4 and Sox2, thereby identifying a direct connection between G1 cyclins and pluripotency factors.
AbstractList Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, upon ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs) phosphorylate and stabilize core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumor-initiating cells, or triple-negative breast cancer cells with a CDK-inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK-inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumor-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.
Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.
Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential. Liu et al.  show that G1 cyclins and their cyclin-dependent kinases regulate the pluripotent state by driving phosphorylation of Nanog, Oct4 and Sox2, thereby identifying a direct connection between G1 cyclins and pluripotency factors.
Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at least one of these cyclin families must be present to allow cell proliferation. Here, we show that several cell types can proliferate in the absence of all G1 cyclins. However, following ablation of G1 cyclins, embryonic stem (ES) cells attenuated their pluripotent characteristics, with the majority of cells acquiring the trophectodermal cell fate. We established that G1 cyclins, together with their associated cyclin-dependent kinases (CDKs), phosphorylate and stabilize the core pluripotency factors Nanog, Sox2 and Oct4. Treatment of murine ES cells, patient-derived glioblastoma tumour-initiating cells, or triple-negative breast cancer cells with a CDK inhibitor strongly decreased Sox2 and Oct4 levels. Our findings suggest that CDK inhibition might represent an attractive therapeutic strategy by targeting glioblastoma tumour-initiating cells, which depend on Sox2 to maintain their tumorigenic potential.
Audience Academic
Author Ordureau, Alban
Sicinski, Piotr
Shimizu, Kouhei
Inuzuka, Hiroyuki
Ligon, Keith L.
Nihira, Naoe Taira
Geng, Yan
Li, Na
Bronson, Roderick T.
Liu, Lijun
Kołodziejczyk, Aleksandra
Harper, J. Wade
Gygi, Steven P.
Chick, Joel M.
Meng, Alice Y.
Michowski, Wojciech
Polyak, Kornelia
Wei, Wenyi
AuthorAffiliation 2 Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA
8 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA
3 Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
1 Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA
6 Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts 02215, USA
7 Department of Biomedical Sciences, Tufts University Veterinary School, North Grafton, Massachusetts 01536, USA
4 Department of Cell Biology, Harvard Medical School, Boston, Massachusetts 02115, USA
5 Department of Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts 02215, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28192421$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Springer Nature Limited 2017
COPYRIGHT 2017 Nature Publishing Group
Copyright Nature Publishing Group Mar 2017
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Snippet Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by the D-type and E-type cyclins. According to the current models, at...
Progression of mammalian cells through the G1 and S phases of the cell cycle is driven by D-type and E-type cyclins. According to the current models, at least...
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StartPage 177
SubjectTerms 13/1
13/100
13/106
13/2
13/31
13/44
13/51
45/23
45/88
45/91
631/532
631/532/2064/1519
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Analysis
Animals
Biology
Biomarkers - metabolism
Cancer
Cancer Research
Cell Biology
Cell Cycle
Cell Differentiation
Cell growth
Cell Proliferation
Cell Separation
Cyclin G1 - metabolism
Cyclin-dependent kinases
Cyclins
Developmental Biology
DNA - analysis
Embryo, Mammalian - cytology
Embryonic stem cells
Epigenesis, Genetic
Experiments
Female
Flow Cytometry
Gene Expression Profiling
Genetic aspects
Growth
Histones - metabolism
Hormones - pharmacology
Imaging, Three-Dimensional
Kinases
Life Sciences
Lysine - metabolism
Mammary Glands, Animal - cytology
Mammary Glands, Animal - embryology
Methylation
Mice
Mice, Inbred C57BL
Mouse Embryonic Stem Cells - cytology
Mouse Embryonic Stem Cells - metabolism
Pathology
Properties
Proteins
Receptors, G-Protein-Coupled - metabolism
RNA - analysis
Stem Cells
Steroids - pharmacology
Tetraspanins - metabolism
Title G1 cyclins link proliferation, pluripotency and differentiation of embryonic stem cells
URI https://link.springer.com/article/10.1038/ncb3474
https://www.ncbi.nlm.nih.gov/pubmed/28192421
https://www.proquest.com/docview/1892241703
https://www.proquest.com/docview/1868393864
https://www.proquest.com/docview/1897378187
https://pubmed.ncbi.nlm.nih.gov/PMC5489757
Volume 19
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