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Cell stress and MEKK1-mediated c-Jun activation modulate NFkappaB activity and cell viability

AuthorsSánchez-Pérez, Isabel; Aznar, Salvador; Martínez-Gomariz, Montserrat; Lacal, Juan Carlos CSIC ORCID; Perona Abellón, Rosario CSIC ORCID
Issue DateAug-2002
PublisherAmerican Society for Cell Biology
CitationMolecular Biology of the Cell 13(8): 2933-2045 (2002)
AbstractChemotherapeutic 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 NFkappaB. We have found a cross-talk between c-Jun expression and NFkappaB 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 NFkappaB-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 NFkappaB-dependent transcription by c-jun contributes to cisplatin-induced cell death, which suggests that inhibition of NFkappaB may potentiate the antineoplastic effect of conventional chemotherapeutic agents.
Description13 pages, 11 figures.
Publisher version (URL)–01–0022.
Appears in Collections:(IIBM) Artículos

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