Interaction of p53 with tumor suppressive and oncogenic signaling pathways to control cellular reactive oxygen species production.
Antioxid Redox Signal
; 15(6): 1749-61, 2011 Sep 15.
Article
em En
| MEDLINE
| ID: mdl-20919943
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/ß-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-ß (TGF-ß) and stress-activated protein kinases (SAPK) that produce ROS, to stop or eliminate uncontrolled proliferating cells.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteína Supressora de Tumor p53
/
Fator de Crescimento Transformador beta
/
Espécies Reativas de Oxigênio
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Neoplasias
Tipo de estudo:
Prognostic_studies
Limite:
Humans
Idioma:
En
Revista:
Antioxid Redox Signal
Assunto da revista:
METABOLISMO
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
Argentina
País de publicação:
Estados Unidos