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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells

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Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells

dc.contributor.author	García Valero, Juan	es_ES
dc.contributor.author	Sancey, Lucie	es_ES
dc.contributor.author	Kucharczak, Jérôme	es_ES
dc.contributor.author	Guillemin, Yannis	es_ES
dc.contributor.author	Gimenez, Diana	es_ES
dc.contributor.author	Prudent, Julien	es_ES
dc.contributor.author	Gillet, Germain	es_ES
dc.contributor.author	Salgado Benito, Jesús	es_ES
dc.contributor.author	Coll, Jean-Luc	es_ES
dc.contributor.author	Aouacheria, Abdel	es_ES
dc.date.accessioned	2015-06-22T09:46:03Z
dc.date.available	2015-06-22T09:46:03Z
dc.date.issued	2011	es_ES
dc.identifier.citation	Journal of Cell Science Vol. 124 Issue Pt 4: pp. 556-564	es_ES
dc.identifier.uri	http://hdl.handle.net/10550/44649
dc.description.abstract	SUMMARYAlthough many cancer cells are primed for apoptosis, they usually develop resistance to cell death at multiple levels. Permeabilization of the outer mitochondrial membrane, which is mediated by proapoptotic Bcl-2 family members like Bax, is considered as a point-of-no-return for initiating apoptotic cell death. This crucial role has placed Bcl-2 family proteins as recurrent targets for anticancer drug development. Here, we propose and demonstrate a new concept based on using minimal active version of Bax to induce cell death independently of endogenous Bcl-2 proteins. We show that membrane-active segments of Bax can directly induce the release of mitochondria-residing apoptogenic factors and commit tumor cells promptly and irreversibly to caspase-dependent apoptosis. On this basis, we designed a peptide encompassing part of the Bax pore-forming domain, able to target mitochondria, induce cytochrome c release and trigger caspase-dependent apoptosis. Moreover, this Bax-derived poropeptide produced effective tumor regression after peritumoral injection in a nude mouse xenograft model. Thus, peptides derived from proteins evolutionary functionalized to form pores in the mitochondrial outer membrane represent novel templates for anticancer agents.	es_ES
dc.subject	Animals	es_ES
dc.subject	Antineoplastic Agents	es_ES
dc.subject	chemistry	es_ES
dc.subject	metabolism	es_ES
dc.subject	pharmacology	es_ES
dc.subject	Apoptosis	es_ES
dc.subject	drug effects	es_ES
dc.subject	Cell Line, Tumor	es_ES
dc.subject	Cytochromes c	es_ES
dc.subject	metabolism	es_ES
dc.subject	Humans	es_ES
dc.subject	Mice	es_ES
dc.subject	Mitochondria	es_ES
dc.subject	drug effects	es_ES
dc.subject	metabolism	es_ES
dc.subject	Neoplasms	es_ES
dc.subject	drug therapy	es_ES
dc.subject	physiopathology	es_ES
dc.subject	Peptides	es_ES
dc.subject	chemistry	es_ES
dc.subject	genetics	es_ES
dc.subject	metabolism	es_ES
dc.subject	pharmacology	es_ES
dc.subject	Protein Structure, Tertiary	es_ES
dc.subject	bcl-2-Associated X Protein	es_ES
dc.subject	chemistry	es_ES
dc.subject	genetics	es_ES
dc.subject	metabolism	es_ES
dc.subject	pharmacology	es_ES
dc.subject	apoptosis	es_ES
dc.subject	Bcl-2 family	es_ES
dc.subject	proapoptotic Bax	es_ES
dc.subject	mitochondria	es_ES
dc.subject	pore-forming peptides	es_ES
dc.subject	anticancer agent	es_ES
dc.subject	antivascular therapy	es_ES
dc.title	Bax-derived membrane-active peptides act as potent and direct inducers of apoptosis in cancer cells	es_ES
dc.type	journal article	es_ES
dc.identifier.doi	10.1242/jcs.076745	es_ES
dc.identifier.idgrec	063425	es_ES