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Mutant p53 facilitates pro-angiogenic, hyperproliferative phenotype in response to chronic relative hypoxia

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Kamat, Chandrashekhar D., Green, Dixy E., Warnke, Linda, Thorpe, Jessica E., Ceriello, Antonio and Ihnat, Michael A. (2007) Mutant p53 facilitates pro-angiogenic, hyperproliferative phenotype in response to chronic relative hypoxia. Cancer Letters, Vol.249 (No.2). pp. 209-219. doi:10.1016/j.canlet.2006.08.017

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Official URL: http://dx.doi.org/10.1016/j.canlet.2006.08.017

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Abstract

There is much controversy in the literature regarding the role of p53 status response on hypoxia inducible factor (HIF) signaling in response to chronic relative hypoxia (CRH). The goal of this paper was to methodically examine this response in isogenically matched tumor cells. We report that p53-mutant (MUT) cells, versus p53-wild-type (WT) cells, showed decreased apoptosis, increased cell proliferation with higher basal HIF-1 alpha levels in response to CRH. In addition, we found increased HIF-mediated transactivation and increased VEGF release with decreased HIF-1 alpha/p53 and HIF-1 alpha/ MDM-2 partnering in p53-MUT versus p53-WT cells in response to CRH. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

Item Type: Journal Article
Subjects: R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Divisions: Faculty of Medicine > Warwick Medical School
Journal or Publication Title: Cancer Letters
Publisher: Elsevier Ireland Ltd.
ISSN: 0304-3835
Official Date: 8 May 2007
Dates:
DateEvent
8 May 2007Published
Volume: Vol.249
Number: No.2
Number of Pages: 11
Page Range: pp. 209-219
DOI: 10.1016/j.canlet.2006.08.017
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Restricted or Subscription Access

Data sourced from Thomson Reuters' Web of Knowledge

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