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Vol. 13, Issue 8, 2933-2945, August 2002
B Activity and Cell Viability
Instituto de Investigaciones Biomédicas Consejo Superior de
Investigaciones Cientificas-Universidad Autónoma de
Madrid, 28029 Madrid, Spain
Chemotherapeutic agents such as cisplatin induce persistent
activation of N-terminal c-Jun Kinase, which in turn mediates induction
of apoptosis. By using a common MAPK Kinase, MEKK1, cisplatin also
activates the survival transcription factor NF
B. 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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