Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production

Autores
Ladelfa, Maria Fatima; Toledo, Maria Fernanda; Laiseca, Julieta Eva; Monte, Martin
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
p53 is a crucial transcription factor with tumor suppressive properties that elicits its function through specific target genes. It constitutes a pivotal system that integrates information received by many signaling pathways and subsequently orchestrates cell fate decisions, namely, growth-arrest, senescence, or apoptosis. Reactive oxygen species (ROS) production in cells can play a key role in signal transduction, being able to trigger different processes as cell death or cell proliferation. Sustained oxidative stress can induce genomic instability and collaborates with cancer development, whereas acute enhancement of high ROS levels leads to toxic oxidative cell damage and cell death. Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Further, we have discussed how p53 could play a role in preventing potentially harmful oxidative state and cell proliferation by pro-oncogenic pathways such as PI3K/AKT/mTOR and WNT/β-catenin or under hypoxia state. In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-β (TGF-β) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells. © 2011 Mary Ann Liebert, Inc.
Fil: Ladelfa, Maria Fatima. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Toledo, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Laiseca, Julieta Eva. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Materia
P53
Ros
Signalling
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/66762
Acceder
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network_name_str CONICET Digital (CONICET)
spelling Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species productionLadelfa, Maria FatimaToledo, Maria FernandaLaiseca, Julieta EvaMonte, MartinP53RosSignallinghttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1p53 is a crucial transcription factor with tumor suppressive properties that elicits its function through specific target genes. It constitutes a pivotal system that integrates information received by many signaling pathways and subsequently orchestrates cell fate decisions, namely, growth-arrest, senescence, or apoptosis. Reactive oxygen species (ROS) production in cells can play a key role in signal transduction, being able to trigger different processes as cell death or cell proliferation. Sustained oxidative stress can induce genomic instability and collaborates with cancer development, whereas acute enhancement of high ROS levels leads to toxic oxidative cell damage and cell death. Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Further, we have discussed how p53 could play a role in preventing potentially harmful oxidative state and cell proliferation by pro-oncogenic pathways such as PI3K/AKT/mTOR and WNT/β-catenin or under hypoxia state. In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-β (TGF-β) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells. © 2011 Mary Ann Liebert, Inc.Fil: Ladelfa, Maria Fatima. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Toledo, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Laiseca, Julieta Eva. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; ArgentinaFil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; ArgentinaMary Ann Liebert2011-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/66762Ladelfa, Maria Fatima; Toledo, Maria Fernanda; Laiseca, Julieta Eva; Monte, Martin; Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production; Mary Ann Liebert; Antioxidants & Redox Signaling; 15; 6; 9-2011; 1749-17611523-0864CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1089/ars.2010.3652info:eu-repo/semantics/altIdentifier/url/https://www.liebertpub.com/doi/10.1089/ars.2010.3652info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:09:34Zoai:ri.conicet.gov.ar:11336/66762instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:09:35.059CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
title Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
spellingShingle Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
Ladelfa, Maria Fatima
P53
Ros
Signalling
title_short Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
title_full Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
title_fullStr Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
title_full_unstemmed Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
title_sort Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
dc.creator.none.fl_str_mv Ladelfa, Maria Fatima
Toledo, Maria Fernanda
Laiseca, Julieta Eva
Monte, Martin
author Ladelfa, Maria Fatima
author_facet Ladelfa, Maria Fatima
Toledo, Maria Fernanda
Laiseca, Julieta Eva
Monte, Martin
author_role author
author2 Toledo, Maria Fernanda
Laiseca, Julieta Eva
Monte, Martin
author2_role author
author
author
dc.subject.none.fl_str_mv P53
Ros
Signalling
topic P53
Ros
Signalling
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv p53 is a crucial transcription factor with tumor suppressive properties that elicits its function through specific target genes. It constitutes a pivotal system that integrates information received by many signaling pathways and subsequently orchestrates cell fate decisions, namely, growth-arrest, senescence, or apoptosis. Reactive oxygen species (ROS) production in cells can play a key role in signal transduction, being able to trigger different processes as cell death or cell proliferation. Sustained oxidative stress can induce genomic instability and collaborates with cancer development, whereas acute enhancement of high ROS levels leads to toxic oxidative cell damage and cell death. Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Further, we have discussed how p53 could play a role in preventing potentially harmful oxidative state and cell proliferation by pro-oncogenic pathways such as PI3K/AKT/mTOR and WNT/β-catenin or under hypoxia state. In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-β (TGF-β) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells. © 2011 Mary Ann Liebert, Inc.
Fil: Ladelfa, Maria Fatima. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Toledo, Maria Fernanda. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Laiseca, Julieta Eva. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
Fil: Monte, Martin. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Química Biológica. Laboratorio de Biología Celular y Molecular; Argentina
description p53 is a crucial transcription factor with tumor suppressive properties that elicits its function through specific target genes. It constitutes a pivotal system that integrates information received by many signaling pathways and subsequently orchestrates cell fate decisions, namely, growth-arrest, senescence, or apoptosis. Reactive oxygen species (ROS) production in cells can play a key role in signal transduction, being able to trigger different processes as cell death or cell proliferation. Sustained oxidative stress can induce genomic instability and collaborates with cancer development, whereas acute enhancement of high ROS levels leads to toxic oxidative cell damage and cell death. Here, it has been considered p53 broad potential contribution through its ability to regulate selected key cancer signaling pathways, where ROS participate as inductors or effectors of the final biological outcome. Further, we have discussed how p53 could play a role in preventing potentially harmful oxidative state and cell proliferation by pro-oncogenic pathways such as PI3K/AKT/mTOR and WNT/β-catenin or under hypoxia state. In addition, we have considered potential mechanisms by which p53 could collaborate with signal transduction pathways such as transforming growth factor-β (TGF-β) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells. © 2011 Mary Ann Liebert, Inc.
publishDate 2011
dc.date.none.fl_str_mv 2011-09
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/66762
Ladelfa, Maria Fatima; Toledo, Maria Fernanda; Laiseca, Julieta Eva; Monte, Martin; Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production; Mary Ann Liebert; Antioxidants & Redox Signaling; 15; 6; 9-2011; 1749-1761
1523-0864
CONICET Digital
CONICET
url http://hdl.handle.net/11336/66762
identifier_str_mv Ladelfa, Maria Fatima; Toledo, Maria Fernanda; Laiseca, Julieta Eva; Monte, Martin; Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production; Mary Ann Liebert; Antioxidants & Redox Signaling; 15; 6; 9-2011; 1749-1761
1523-0864
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1089/ars.2010.3652
info:eu-repo/semantics/altIdentifier/url/https://www.liebertpub.com/doi/10.1089/ars.2010.3652
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Mary Ann Liebert
publisher.none.fl_str_mv Mary Ann Liebert
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.13397

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