Skip to Main content Skip to Navigation
Theses

RÉPONSE À LA CHIMIOTHÉRAPIE ET PROGRESSION DU CYCLE CELLULAIRE : RÔLE DE L'ONCOGÈNE STAT3 DANS LE CANCER COLORECTAL

Abstract : The STAT3 transcription factor are cytoplasmic proteins that induce gene activation in response to growth factor stimulation or cytokines. Following tyrosine phosphorylation, STAT3 proteins dimerize, translocate to the nucleus and activate specific target genes involved in cell cycle progression from G1 to S phase. We observed that STAT3 is phosphorylated on its residue serine 727 by the Cdk5 kinase in response to topoisomerase I inhibition. The pathway Cdk5-STAT3 is involved in the down-regulation of early G1 genes as Cyclin D1 and c-Myc and in up-regulation of the Eme1 gene, an endonuclease involved in the processing of damaged replication forks. Moreover, we showed that STAT3 is also phosphorylated on its residue serine 727 during G2 phase and mitosis. STAT3 is phosphorylated by the Cdk1 kinase to regulates the expression of genes involved in the progression from G2 to M phase such as PLK1, STIL,RIC8A, FoxM1, NuMa, Cdc25C. Using immunohistochemistry analysis, we observed that STAT3 is phosphorylated on its residue serine 727 in early stage of colorectal cancer. This phosphorylation activates two different pathways : DNA repair following genotoxic treatment and cell cycle progression from G2 to mitosis.
Document type :
Theses
Complete list of metadata

https://tel.archives-ouvertes.fr/tel-00979247
Contributor : Anne-Marie Plé <>
Submitted on : Tuesday, April 15, 2014 - 3:47:31 PM
Last modification on : Tuesday, April 15, 2014 - 4:43:01 PM
Long-term archiving on: : Tuesday, July 15, 2014 - 11:15:31 AM

Identifiers

  • HAL Id : tel-00979247, version 1

Collections

Citation

Hélène Sellier. RÉPONSE À LA CHIMIOTHÉRAPIE ET PROGRESSION DU CYCLE CELLULAIRE : RÔLE DE L'ONCOGÈNE STAT3 DANS LE CANCER COLORECTAL. Biologie cellulaire. Université d'Angers, 2011. Français. ⟨tel-00979247⟩

Share

Metrics

Record views

857

Files downloads

1513