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A more recent version of this article appeared on August 1, 2002
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Submitted on January 15, 2002
Revised on April 29, 2002
Accepted on May 31, 2002
B activity and cell viability
1 Instituto de Investigaciones Biomédicas C.S.I.C.-UAM,
C/ Arturo Duperier, 4, 28029 Madrid, Spain
2 Instituto de Investigaciones Biomédicas C.S.I.C.-UAM, C/ Arturo Duperier, 4, 28029 Madrid, Spain
* Corresponding author. E-mail address: RPerona{at}iib.uam.es.
Chemotherapeutic agents such as cisplatin induce persistent activation of N-terminal c-Jun Kinase, who in turn mediates induction of apoptosis. By using a common MAPK Kinase, MEKK1, cisplatin also activates the survival transcription factor NFB. We have found a cross talk between c-Jun expression and NFB transcriptional activation in response to cisplatin. Fibroblast derived from c-jun knock out mice are more resistant to cisplatin induced cell death, and this survival advantage is mediated by upregulation of NFB dependent transcription and expression of MIAP3. This process can be reverted by ectopic expression of c-Jun in c-jun-/- fibroblasts, which decreases p65 transcriptional activity back to normal levels. Negative regulation of NFB dependent transcription by c-jun contributes to cisplatin induced cell death, which suggests that inhibition of NFB may potentiate the antineoplastic effect of conventional chemotherapeutic agents.
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