cisplatinum and taxol induce different patterns of p53 phosphorylation

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ID: 181286
2001
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Abstract
Posttranslational modifications of p53 induced by two widely used anticancer agents, cisplatinum (DDP) and taxol were investigated in two human cancer cell lines. Although both drugs were able to induce phosphorylation at serine 20 (Ser20), only DDP treatment induced p53 phosphorylation at serine 15 (Ser15). Moreover, both drug treatments were able to increase p53 levels and consequently the transcription of waf1 and mdm-2 genes, although DDP treatment resulted in a stronger inducer of both genes. Using two ataxia telangiectasia mutated (ATM) cell lines, the role of ATM in druginduced p53 phosphorylations was investigated. No differences in drug-induced p53 phosphorylation could be observed, indicating that ATM is not the kinase involved in these phosphorylation events. In addition, inhibition of DNA-dependent protein kinase activity by wortmannin did not abolish p53 phosphorylation at Ser15 and Ser20, again indicating that DNA-PK is unlikely to be the kinase involved. After both taxol and DDP treatments, an activation of hCHK2 was found and this is likely to be responsible for phosphorylation at Ser20. In contrast, only DDP was able to activate ATR, which is the candidate kinase for phosphorylation of Ser15 by this drug. This data clearly suggests that differential mechanisms are involved in phosphorylation and activation of p53 depending on the drug type.
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damia2001neoplasia:cisplatinum Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Giovanna Damia;Laura Filiberti;Faina Vikhanskaya;Laura Carrassa;Yoichi Taya;Maurizio Dincalci;Massimo Broggini
Journal ACS chemical neuroscience
Year 2001
DOI
10.1038/sj.neo.7900122
URL
http://www.sciencedirect.com/science/article/pii/S1476558601800117
Keywords
cell cycle phosphorylation anticancer agents Oncology including cancer and carcinogens tumors

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