Cross-talk between HIF and p53 as mediators of molecular responses to physiological and genotoxic stresses

Molecular Cancer

Review

Silvia Pastorekova¹  Borek Vojtesek²  Roman Hrstka²  Joanna Obacz³ 

[1] Department of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences, Dubravska cesta 9, 84505, Bratislava, Slovak Republic;Masaryk Memorial Cancer Institute, Regional Centre for Applied Molecular Oncology, Zluty kopec 7, 65653, Brno, Czech Republic;Masaryk Memorial Cancer Institute, Regional Centre for Applied Molecular Oncology, Zluty kopec 7, 65653, Brno, Czech Republic;Department of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences, Dubravska cesta 9, 84505, Bratislava, Slovak Republic;

关键词: p53;    HIF-1;    Hypoxia;    DNA damage;    Cancer;   

DOI  :  10.1186/1476-4598-12-93

 received in 2013-04-23, accepted in 2013-08-10,  发布年份 2013

来源: Springer

【 摘 要 】

Abnormal rates of growth together with metastatic potential and lack of susceptibility to cellular signals leading to apoptosis are widely investigated characteristics of tumors that develop via genetic or epigenetic mechanisms. Moreover, in the growing tumor, cells are exposed to insufficient nutrient supply, low oxygen availability (hypoxia) and/or reactive oxygen species. These physiological stresses force them to switch into more adaptable and aggressive phenotypes. This paper summarizes the role of two key mediators of cellular stress responses, namely p53 and HIF, which significantly affect cancer progression and compromise treatment outcomes. Furthermore, it describes cross-talk between these factors.

【 授权许可】

Unknown   
© Obacz et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.