Aplidin® induces JNK-dependent apoptosis in human breast cancer cells via alteration of glutathione homeostasis, Rac1 GTPase activation, and MKP-1 phosphatase ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2006-11

AUTHORS

L González-Santiago, Y Suárez, N Zarich, M J Muñoz-Alonso, A Cuadrado, T Martínez, L Goya, A Iradi, G Sáez-Tormo, J V Maier, A Moorthy, A C B Cato, J M Rojas, A Muñoz

ABSTRACT

Aplidin is an antitumor agent in phase II clinical trials that induces apoptosis through the sustained activation of Jun N-terminal kinase (JNK). We report that Aplidin alters glutathione homeostasis increasing the ratio of oxidized to reduced forms (GSSG/GSH). Aplidin generates reactive oxygen species and disrupts the mitochondrial membrane potential. Exogenous GSH inhibits these effects and also JNK activation and cell death. We found two mechanisms by which Aplidin activates JNK: rapid activation of Rac1 small GTPase and downregulation of MKP-1 phosphatase. Rac1 activation was diminished by GSH and enhanced by L-buthionine (SR)-sulfoximine, which inhibits GSH synthesis. Downregulation of Rac1 by transfection of small interfering RNA (siRNA) duplexes or the use of a specific Rac1 inhibitor decreased Aplidin-induced JNK activation and cytotoxicity. Our results show that Aplidin induces apoptosis by increasing the GSSG/GSH ratio, a necessary step for induction of oxidative stress and sustained JNK activation through Rac1 activation and MKP-1 downregulation. More... »

PAGES

4401898

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.cdd.4401898

DOI

http://dx.doi.org/10.1038/sj.cdd.4401898

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009618114

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16543941


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