Fiche publication
Journal
Biology of the cell
Auteurs
Membres identifiés du Cancéropôle Est :
Pr PRETET Jean-Luc
Tous les auteurs :
Bernard B, Prétet JL, Charlot JF, Mougin C
Lien Pubmed
Résumé
We have recently shown that staurosporine (ST) can trigger apoptosis of CaSki and HeLa cervical tumor cells from G2/M checkpoint, though the mechanism remains elusive. In this study, we reported that ST induced the inhibition of E6 and E7 viral oncogene and MDM2 expression, while it led to increased levels of p53, which was transiently located to mitochondria. Additionally, the proteins of the p53-regulated genes, p21(WAF1) and Bax, were increased with a similar time, while Bcl-2 and Bcl-X(L) expression was lowered. Upon ST treatment, the cytochrome c was released into the cytosol and, then, activation of caspases-9 and -3 led to Poly(ADP)RibosePolymerase (PARP) cleavage. Finally, characteristic morphological signs confirmed the apoptosis execution. Thus, taken together, all these observations suggest that apoptosis can be reactivated in HPV-positive human carcinoma cells and highlight that ST could be used as a potently chemotherapy agent to enhance the sensitivity of tumor cells to apoptosis.
Mots clés
Animals, Apoptosis, drug effects, Blotting, Western, DNA-Binding Proteins, Enzyme Inhibitors, pharmacology, Female, Genes, p53, drug effects, HeLa Cells, Humans, Nuclear Proteins, Oncogene Proteins, Viral, drug effects, Papillomaviridae, drug effects, Papillomavirus Infections, drug therapy, Proto-Oncogene Proteins, drug effects, Proto-Oncogene Proteins c-mdm2, Repressor Proteins, Reverse Transcriptase Polymerase Chain Reaction, Staurosporine, pharmacology, Tumor Virus Infections, drug therapy, Uterine Cervical Neoplasms, drug therapy
Référence
Biol. Cell. ;95(1):17-26
