Please use this identifier to cite or link to this item: http://hdl.handle.net/2067/43497
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dc.contributor.authorMuñoz, Diegoit
dc.contributor.authorBrucoli, Martinait
dc.contributor.authorZecchini, Silviait
dc.contributor.authorSandoval-Hernandez, Adrianit
dc.contributor.authorArboleda, Gonzaloit
dc.contributor.authorLopez-Vallejo, Fabianit
dc.contributor.authorDelgado, Wilmanit
dc.contributor.authorGiovarelli, Matteoit
dc.contributor.authorCoazzoli, Marcoit
dc.contributor.authorCatalani, Elisabettait
dc.contributor.authorDe Palma, Clarait
dc.contributor.authorPerrotta, Cristianait
dc.contributor.authorCuca, Luisit
dc.contributor.authorClementi, Emilioit
dc.contributor.authorCervia, Davideit
dc.date.accessioned2021-06-11T10:29:38Z-
dc.date.available2021-06-11T10:29:38Z-
dc.date.issued2019it
dc.identifier.issn2072-6694it
dc.identifier.urihttp://hdl.handle.net/2067/43497-
dc.description.abstractX-linked inhibitor of apoptosis protein (XIAP) is an emerging crucial therapeutic target in cancer. We report on the discovery and characterisation of small organic molecules from Piper genus plants exhibiting XIAP antagonism, namely erioquinol, a quinol substituted in the 4-position with an alkenyl group and the alkenylphenols eriopodols A-C. Another isolated compound was originally identified as gibbilimbol B. Erioquinol was the most potent inhibitor of human cancer cell viability when compared with gibbilimbol B and eriopodol A was listed as intermediate. Gibbilimbol B and eriopodol A induced apoptosis through mitochondrial permeabilisation and caspase activation while erioquinol acted on cell fate via caspase-independent/non-apoptotic mechanisms, likely involving mitochondrial dysfunctions and aberrant generation of reactive oxygen species. In silico modelling and molecular approaches suggested that all molecules inhibit XIAP by binding to XIAP-baculoviral IAP repeat domain. This demonstrates a novel aspect of XIAP as a key determinant of tumour control, at the molecular crossroad of caspase-dependent/independent cell death pathway and indicates molecular aspects to develop tumour-effective XIAP antagonists.it
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/us/*
dc.titleXIAP as a Target of New Small Organic Natural Molecules Inducing Human Cancer Cell Deathit
dc.typearticle*
dc.identifier.doi10.3390/cancers11091336it
dc.identifier.pmid31505859it
dc.identifier.scopus2-s2.0-85073331569it
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/85073331569it
dc.relation.journalCANCERSit
dc.relation.firstpage1336it
dc.relation.volume11it
dc.relation.issue9it
dc.type.miur262*
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.grantfulltextrestricted-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.journal.journalissn2072-6694-
crisitem.journal.anceE202438-
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