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Implication de l'oncogène STAT3 dans la réponse aux traitements de chimiothérapies : Application au cancer colorectal

Abstract : STAT3 transcription factors are activated and involved in tumor development. Phosphorylation of STAT3 on tyrosine 705 is involved in cell transformation and in the exhaust of conventional chemotherapy treatment. The involvement of the 2nd site of phosphorylation of STAT3 on serine 727, in responseto treatment has been little studied. Inhibition of topoisomerases leads to the activation of cdk5 kinase that phosphorylates STAT3 on its serine residue. STAT3 will bind to the promoter of the Eme1 gene to activate transcription. Eme is a protein involves in the DNA damage repair. This allows repair of DNA damage induced by SN38 and resulted in a decreased sensitivity to treatment. No tyrosine phosphorylation was observed under these conditions and the genes of cyclin D1 and myc are not transcribed. But myc is recruited to the promoter of Aurora A in G2/M phase. The irinotecan by inhibiting myc, results in a loss of transcription of Aurora A and leeds to cell cycle arrest. STAT3 phosphorylation on its serine residue could be involved in the induction of senescence and in the repair of DNA damage. The celle diverting the process of protecting against tumor development to create resistance to treatment. The detection of this phosphorylation could thus predict the response of patients to treatment.
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Submitted on : Tuesday, March 15, 2011 - 12:19:19 PM
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Sandy Courapied. Implication de l'oncogène STAT3 dans la réponse aux traitements de chimiothérapies : Application au cancer colorectal. Biologie cellulaire. Université d'Angers, 2010. Français. ⟨tel-00576728⟩

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