Journal
FEBS LETTERS
Volume 583, Issue 22, Pages 3557-3562Publisher
WILEY
DOI: 10.1016/j.febslet.2009.10.059
Keywords
Esophageal carcinoma; Focal adhesion kinase; p53; Apoptosis
Funding
- National Research Foundation (NRF)
- HE Griffin Cancer Trust
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A novel survival role of focal adhesion kinase (FAK) that involves its nuclear translocation and direct association with p53 has been demonstrated. Here we examined the relationship between the p53/FAK interaction and Ser46 phosphorylation of p53 (p-p53(Ser46)) in the apoptotic regulation of human esophageal squamous cell carcinoma (HOSCC) cell lines, expressing either wild type (wt) p53 or mutant (mt) p53-R175H. In contrast to the wt p53 cell lines, the mt p53-R175H cell line was resistant to staurosporine (STS)-mediated detachment and caspase-3 activation. Furthermore, despite the resistance of mt p53-R175H to Ser46 phosphorylation, both wt and mt HOSCC cells translocate FAK into the nucleus and maintain the p53/FAK interaction post STS treatment. These findings provide unique insight into how tumor cells harboring the R175H mutant may resist chemotherapeutic intervention. Structured summary: MINT-7294020: FAK (uniprotkb:Q05397) physically interacts (MI:0915) with p53 (uniprotkb:P04637) by anti-bait coimmunoprecipitation (MI:0006) (C) 2009 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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