The emerging role of APC/CCdh1 in controlling differentiation, genomic stability and tumor suppression

Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cyc...

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Published inOncogene Vol. 29; no. 1; pp. 1 - 10
Main Authors Wäsch, R, Robbins, J A, Cross, F R
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 07.01.2010
Nature Publishing Group
Subjects
Online AccessGet full text
ISSN0950-9232
1476-5594
1476-5594
DOI10.1038/onc.2009.325

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Abstract Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C Cdh1 is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.
AbstractList Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C(Cdh1) is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C(Cdh1) is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.
Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C(Cdh1) is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.
Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell cycle regulators and also inhibitors of differentiation, coupling cell cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell cycle re-entry and either perturbed differentiation or dedifferentiation. Additionally, APC/CCdh1 is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.
Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C(Cdh1) is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells. [PUBLICATION ABSTRACT]
Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell-cycle exit and differentiation. The anaphase-promoting complex or cyclosome (APC/C) activated by Cdh1 coordinately eliminates positive cell-cycle regulators as well as inhibitors of differentiation, thereby coupling cell-cycle exit and differentiation. Misregulation of Cdh1 thus has the potential to promote both cell-cycle re-entry and either perturbed differentiation or dedifferentiation. In addition, APC/C Cdh1 is required to maintain genomic stability. As a result, loss of Cdh1 can contribute to tumorigenesis in the form of proliferation of poorly differentiated and genetically unstable cells.
Author Wäsch, R
Robbins, J A
Cross, F R
AuthorAffiliation 1 Department of Hematology and Oncology, University Medical Center, Freiburg, Germany
2 The Rockefeller University, 1230 York Avenue, New York 10065, USA
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  givenname: J A
  surname: Robbins
  fullname: Robbins, J A
  organization: Laboratory of Yeast Molecular Genetics, The Rockefeller University, New York, NY, USA
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  surname: Cross
  fullname: Cross, F R
  organization: Laboratory of Yeast Molecular Genetics, The Rockefeller University, New York, NY, USA
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ISSN 0950-9232
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IngestDate Wed Oct 01 15:56:08 EDT 2025
Tue Sep 30 16:43:34 EDT 2025
Sun Sep 28 10:56:25 EDT 2025
Sat Aug 23 12:53:29 EDT 2025
Mon Jul 21 05:59:08 EDT 2025
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IsDoiOpenAccess true
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Issue 1
Keywords tumor suppression
proteasome
anaphase-promoting complex
differentiation
genomic instability
ubiquitin
Ubiquitin
Multicatalytic endopeptidase complex
Stability
Carbon-nitrogen ligases
Enzyme
Genomics
Suppression
Carcinogenesis
Peptidases
Ligases
Cell cycle
Hydrolases
Instability
Tumor
Differentiation
Ubiquitin-protein ligase
Language English
License CC BY 4.0
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c3895-7b0ca6b546d0aadfd557d01d71de1027b103ac6b0ac435370eeb529310767eac3
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
OpenAccessLink https://proxy.k.utb.cz/login?url=https://www.nature.com/articles/onc2009325.pdf
PMID 19826416
PQID 227366231
PQPubID 36330
PageCount 10
ParticipantIDs unpaywall_primary_10_1038_onc_2009_325
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pascalfrancis_primary_22323245
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ProviderPackageCode CITATION
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PublicationCentury 2000
PublicationDate 20100107
PublicationDateYYYYMMDD 2010-01-07
PublicationDate_xml – month: 1
  year: 2010
  text: 20100107
  day: 7
PublicationDecade 2010
PublicationPlace London
PublicationPlace_xml – name: London
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PublicationTitle Oncogene
PublicationTitleAbbrev Oncogene
PublicationTitleAlternate Oncogene
PublicationYear 2010
Publisher Nature Publishing Group UK
Nature Publishing Group
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
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Snippet Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to...
Deregulation of the G1/G0 phase of the cell cycle can lead to cancer. During G1, most cells commit alternatively to DNA replication and division, or to cell...
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SubjectTerms Anaphase-Promoting Complex-Cyclosome
Animals
Apoptosis
Biological and medical sciences
Cell Biology
Cell cycle
Cell Cycle - physiology
Cell Cycle Proteins - metabolism
Cell Cycle Proteins - physiology
Cell cycle, cell proliferation
Cell Differentiation - physiology
Cell physiology
Cell Proliferation
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cellular biology
Deoxyribonucleic acid
Diverse techniques
DNA
Fundamental and applied biological sciences. Psychology
Genomic Instability
Genomics
Human Genetics
Humans
Internal Medicine
Medicine
Medicine & Public Health
Models, Biological
Molecular and cellular biology
Neoplasms - genetics
Neoplasms - pathology
Neoplasms - physiopathology
Oncology
review
Ubiquitin-Protein Ligase Complexes - metabolism
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