Notch Signaling Mediates Secondary Senescence

Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally dis...

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Vydané v:	Cell reports (Cambridge) Ročník 27; číslo 4; s. 997 - 1007.e5
Hlavní autori:	Teo, Yee Voan, Rattanavirotkul, Nattaphong, Olova, Nelly, Salzano, Angela, Quintanilla, Andrea, Tarrats, Nuria, Kiourtis, Christos, Müller, Miryam, Green, Anthony R., Adams, Peter D., Acosta, Juan-Carlos, Bird, Thomas G., Kirschner, Kristina, Neretti, Nicola, Chandra, Tamir
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States Elsevier Inc 23.04.2019 Cell Press
Predmet:	Animals bystander senescence CEBPB Cells, Cultured Cellular Senescence Humans Mice, Inbred C57BL Notch oncogene induced senescence Oncogenes - physiology paracrine senescence Receptors, Notch - metabolism Receptors, Notch - physiology secondary senescence senescence senescence associated secretory phenotype Signal Transduction Single-Cell Analysis single-cell RNA sequencing TGFB Transcriptome single-cell RNA sequencing senescence CEBPB secondary senescence senescence associated secretory phenotype Notch paracrine senescence TGFB oncogene induced senescence bystander senescence
ISSN:	2211-1247, 2211-1247
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Abstract	Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence. [Display omitted] •Primary senescence and secondary senescence are distinct molecular endpoints•Secondary Ras-induced senescence has a composite SASP, Notch-induced signature•Notch signaling is an essential driver of secondary senescence•Notch blunts the senescence-associated secretory phenotype in secondary senescence Teo et al. found that secondary senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. The authors show that primary and secondary senescence are distinct molecular endpoints. A blunted secretory phenotype and the induction of fibrillar collagens in secondary senescence point toward functional diversification.
AbstractList	Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence. • Primary senescence and secondary senescence are distinct molecular endpoints • Secondary Ras-induced senescence has a composite SASP, Notch-induced signature • Notch signaling is an essential driver of secondary senescence • Notch blunts the senescence-associated secretory phenotype in secondary senescence Teo et al. found that secondary senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. The authors show that primary and secondary senescence are distinct molecular endpoints. A blunted secretory phenotype and the induction of fibrillar collagens in secondary senescence point toward functional diversification. Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence.Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence. Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence. Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors of the senescence-associated secretory phenotype (SASP). Currently, primary and secondary senescent cells are not considered functionally distinct endpoints. Using single-cell analysis, we observed two distinct transcriptional endpoints, a primary endpoint marked by Ras and a secondary endpoint marked by Notch activation. We find that secondary oncogene-induced senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. Moreover, Notch signaling weakens, but does not abolish, SASP in secondary senescence. Global transcriptomic differences, a blunted SASP response, and the induction of fibrillar collagens in secondary senescence point toward a functional diversification between secondary and primary senescence. [Display omitted] •Primary senescence and secondary senescence are distinct molecular endpoints•Secondary Ras-induced senescence has a composite SASP, Notch-induced signature•Notch signaling is an essential driver of secondary senescence•Notch blunts the senescence-associated secretory phenotype in secondary senescence Teo et al. found that secondary senescence in vitro and in vivo requires Notch, rather than SASP alone, as previously thought. The authors show that primary and secondary senescence are distinct molecular endpoints. A blunted secretory phenotype and the induction of fibrillar collagens in secondary senescence point toward functional diversification.
Author	Neretti, Nicola Green, Anthony R. Adams, Peter D. Chandra, Tamir Bird, Thomas G. Rattanavirotkul, Nattaphong Quintanilla, Andrea Teo, Yee Voan Müller, Miryam Kiourtis, Christos Acosta, Juan-Carlos Tarrats, Nuria Salzano, Angela Kirschner, Kristina Olova, Nelly
AuthorAffiliation	6 Wellcome/MRC Cambridge Stem Cell Institute and Department of Haematology, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK 2 Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02903, USA 4 CRUK Beatson Institute, Glasgow G61 1BD, UK 7 Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA 1 MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK 9 Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK 8 Center for Computational Molecular Biology, Brown University, Providence, RI 02906, USA 5 MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh EH164TJ, UK 3 Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
AuthorAffiliation_xml	– name: 5 MRC Centre for Inflammation Research, University of Edinburgh, Edinburgh EH164TJ, UK – name: 4 CRUK Beatson Institute, Glasgow G61 1BD, UK – name: 6 Wellcome/MRC Cambridge Stem Cell Institute and Department of Haematology, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK – name: 7 Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA – name: 8 Center for Computational Molecular Biology, Brown University, Providence, RI 02906, USA – name: 2 Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02903, USA – name: 3 Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK – name: 9 Wellcome Sanger Institute, Hinxton, Cambridgeshire CB10 1SA, UK – name: 1 MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK
Author_xml	– sequence: 1 givenname: Yee Voan surname: Teo fullname: Teo, Yee Voan organization: Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02903, USA – sequence: 2 givenname: Nattaphong surname: Rattanavirotkul fullname: Rattanavirotkul, Nattaphong organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 3 givenname: Nelly surname: Olova fullname: Olova, Nelly organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 4 givenname: Angela surname: Salzano fullname: Salzano, Angela organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 5 givenname: Andrea surname: Quintanilla fullname: Quintanilla, Andrea organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 6 givenname: Nuria surname: Tarrats fullname: Tarrats, Nuria organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 7 givenname: Christos surname: Kiourtis fullname: Kiourtis, Christos organization: Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK – sequence: 8 givenname: Miryam surname: Müller fullname: Müller, Miryam organization: CRUK Beatson Institute, Glasgow G61 1BD, UK – sequence: 9 givenname: Anthony R. surname: Green fullname: Green, Anthony R. organization: Wellcome/MRC Cambridge Stem Cell Institute and Department of Haematology, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK – sequence: 10 givenname: Peter D. surname: Adams fullname: Adams, Peter D. organization: Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK – sequence: 11 givenname: Juan-Carlos surname: Acosta fullname: Acosta, Juan-Carlos organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK – sequence: 12 givenname: Thomas G. surname: Bird fullname: Bird, Thomas G. organization: CRUK Beatson Institute, Glasgow G61 1BD, UK – sequence: 13 givenname: Kristina surname: Kirschner fullname: Kirschner, Kristina email: kristina.kirschner@glasgow.ac.uk organization: Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK – sequence: 14 givenname: Nicola surname: Neretti fullname: Neretti, Nicola email: nicola_neretti@brown.edu organization: Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02903, USA – sequence: 15 givenname: Tamir surname: Chandra fullname: Chandra, Tamir email: tamir.chandra@igmm.ed.ac.uk organization: MRC Human Genetics Unit, MRC Institute of Genetics and Molecular Medicine, The University of Edinburgh, Edinburgh, UK
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Keywords	single-cell RNA sequencing senescence CEBPB secondary senescence senescence associated secretory phenotype Notch paracrine senescence TGFB oncogene induced senescence bystander senescence
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Snippet	Oncogene-induced senescence (OIS) is a tumor suppressive response to oncogene activation that can be transmitted to neighboring cells through secreted factors...
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SubjectTerms	Animals bystander senescence CEBPB Cells, Cultured Cellular Senescence Humans Mice, Inbred C57BL Notch oncogene induced senescence Oncogenes - physiology paracrine senescence Receptors, Notch - metabolism Receptors, Notch - physiology secondary senescence senescence senescence associated secretory phenotype Signal Transduction Single-Cell Analysis single-cell RNA sequencing TGFB Transcriptome
Title	Notch Signaling Mediates Secondary Senescence
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