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• W2097171599 abstract "Stathmin is a p53-target gene, frequently overexpressed in late stages of human cancer progression. Type II High Grade Epithelial Ovarian Carcinomas (HG-EOC) represents the only clear exception to this observation. Here, we show that stathmin expression is necessary for the survival of HG-EOC cells carrying a p53 mutant (p53(MUT) ) gene. At molecular level, stathmin favours the binding and the phosphorylation of p53(MUT) by DNA-PKCS , eventually modulating p53(MUT) stability and transcriptional activity. Inhibition of stathmin or DNA-PKCS impaired p53(MUT) -dependent transcription of several M phase regulators, resulting in M phase failure and EOC cell death, both in vitro and in vivo. In primary human EOC a strong correlation exists between stathmin, DNA-PKCS , p53(MUT) overexpression and its transcriptional targets, further strengthening the relevance of the new pathway here described. Overall our data support the hypothesis that the expression of stathmin and p53 could be useful for the identification of high risk patients that will benefit from a therapy specifically acting on mitotic cancer cells." @default.
• W2097171599 created "2016-06-24" @default.
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• W2097171599 date "2013-04-22" @default.
• W2097171599 modified "2023-10-16" @default.
• W2097171599 title "Stathmin regulates mutant p53 stability and transcriptional activity in ovarian cancer" @default.
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• W2097171599 doi "https://doi.org/10.1002/emmm.201201504" @default.
• W2097171599 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3927961" @default.
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• W2097171599 hasPublicationYear "2013" @default.
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