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spelling todo:paper_15230864_v15_n6_p1749_Ladelfa2023-10-03T16:20:49Z Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production Ladelfa, M.F. Toledo, M.F. Laiseca, J.E. Monte, M. beta catenin hypoxia inducible factor mammalian target of rapamycin mitogen activated protein kinase phosphatidylinositol 3 kinase protein kinase B protein p53 reactive oxygen metabolite Smad protein stress activated protein kinase transforming growth factor beta Wnt protein apoptosis cell proliferation human hypoxia metabolic regulation nonhuman priority journal protein function review signal transduction Apoptosis Genomic Instability Humans Hypoxia-Inducible Factor 1, alpha Subunit Mitogen-Activated Protein Kinases Neoplasms Oncogenes Reactive Oxygen Species Signal Transduction TOR Serine-Threonine Kinases Transforming Growth Factor beta Tumor Suppressor Protein p53 Wnt Proteins 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, M.F. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Monte, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_15230864_v15_n6_p1749_Ladelfa
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic beta catenin
hypoxia inducible factor
mammalian target of rapamycin
mitogen activated protein kinase
phosphatidylinositol 3 kinase
protein kinase B
protein p53
reactive oxygen metabolite
Smad protein
stress activated protein kinase
transforming growth factor beta
Wnt protein
apoptosis
cell proliferation
human
hypoxia
metabolic regulation
nonhuman
priority journal
protein function
review
signal transduction
Apoptosis
Genomic Instability
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
Mitogen-Activated Protein Kinases
Neoplasms
Oncogenes
Reactive Oxygen Species
Signal Transduction
TOR Serine-Threonine Kinases
Transforming Growth Factor beta
Tumor Suppressor Protein p53
Wnt Proteins
spellingShingle beta catenin
hypoxia inducible factor
mammalian target of rapamycin
mitogen activated protein kinase
phosphatidylinositol 3 kinase
protein kinase B
protein p53
reactive oxygen metabolite
Smad protein
stress activated protein kinase
transforming growth factor beta
Wnt protein
apoptosis
cell proliferation
human
hypoxia
metabolic regulation
nonhuman
priority journal
protein function
review
signal transduction
Apoptosis
Genomic Instability
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
Mitogen-Activated Protein Kinases
Neoplasms
Oncogenes
Reactive Oxygen Species
Signal Transduction
TOR Serine-Threonine Kinases
Transforming Growth Factor beta
Tumor Suppressor Protein p53
Wnt Proteins
Ladelfa, M.F.
Toledo, M.F.
Laiseca, J.E.
Monte, M.
Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
topic_facet beta catenin
hypoxia inducible factor
mammalian target of rapamycin
mitogen activated protein kinase
phosphatidylinositol 3 kinase
protein kinase B
protein p53
reactive oxygen metabolite
Smad protein
stress activated protein kinase
transforming growth factor beta
Wnt protein
apoptosis
cell proliferation
human
hypoxia
metabolic regulation
nonhuman
priority journal
protein function
review
signal transduction
Apoptosis
Genomic Instability
Humans
Hypoxia-Inducible Factor 1, alpha Subunit
Mitogen-Activated Protein Kinases
Neoplasms
Oncogenes
Reactive Oxygen Species
Signal Transduction
TOR Serine-Threonine Kinases
Transforming Growth Factor beta
Tumor Suppressor Protein p53
Wnt Proteins
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.
format JOUR
author Ladelfa, M.F.
Toledo, M.F.
Laiseca, J.E.
Monte, M.
author_facet Ladelfa, M.F.
Toledo, M.F.
Laiseca, J.E.
Monte, M.
author_sort Ladelfa, M.F.
title Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
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
url http://hdl.handle.net/20.500.12110/paper_15230864_v15_n6_p1749_Ladelfa
work_keys_str_mv AT ladelfamf interactionofp53withtumorsuppressiveandoncogenicsignalingpathwaystocontrolcellularreactiveoxygenspeciesproduction
AT toledomf interactionofp53withtumorsuppressiveandoncogenicsignalingpathwaystocontrolcellularreactiveoxygenspeciesproduction
AT laisecaje interactionofp53withtumorsuppressiveandoncogenicsignalingpathwaystocontrolcellularreactiveoxygenspeciesproduction
AT montem interactionofp53withtumorsuppressiveandoncogenicsignalingpathwaystocontrolcellularreactiveoxygenspeciesproduction
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