Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production
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, s...
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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 |
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1807318625080573952 |