Please use this identifier to cite or link to this item: http://hdl.handle.net/2067/48641
DC FieldValueLanguage
dc.contributor.authorFilippi, Silviait
dc.contributor.authorPaccosi, Elenait
dc.contributor.authorBalzerano, Alessioit
dc.contributor.authorFerretti, Margheritait
dc.contributor.authorPoli, Giuliait
dc.contributor.authorTaborri, Juriit
dc.contributor.authorBrancorsini, Stefanoit
dc.contributor.authorProietti-De-Santis, Lucait
dc.date.accessioned2022-11-25T17:52:08Z-
dc.date.available2022-11-25T17:52:08Z-
dc.date.issued2022it
dc.identifier.issn2072-6694it
dc.identifier.urihttp://hdl.handle.net/2067/48641-
dc.description.abstractBreast cancer (BC) is the most common cancer with the highest frequency of death among women. BC is highly heterogenic at the genetic, biological, and clinical level. Despite the significant improvements in diagnosis and treatments of BC, the high rate of cancer recurrence and resistance to treatment remains a major challenge in clinical practice. This issue is particularly relevant in Triple-Negative Breast Cancer (TNBC) subtype, for which chemotherapy remains the main standard therapeutic approach. Here, we observed that BC cells, belonging to different subtypes, including the TNBC, display an increased expression of Cockayne Syndrome group A (CSA) protein, which is involved in multiple functions such as DNA repair, transcription, mitochondrial homeostasis, and cell division and that recently was found to confer cell robustness when it is up-regulated. We demonstrated that CSA ablation by AntiSense Oligonucleotides (ASOs) drastically impairs tumorigenicity of BC cells by hampering their survival and proliferative capabilities without damaging normal cells. Moreover, suppression of CSA dramatically sensitizes BC cells to platinum and taxane derivatives, which are commonly used for BC first-line therapy, even at very low doses not harmful to normal cells. Finally, CSA ablation restores drug sensitivity in oxaliplatin-resistant cells. Based on these results, we conclude that CSA might be a very attractive target for the development of more effective anticancer therapies.it
dc.language.isoitait
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.titleCSA Antisense Targeting Enhances Anticancer Drug Sensitivity in Breast Cancer Cells, including the Triple-Negative Subtypeit
dc.typearticle*
dc.identifier.doi10.3390/cancers14071687it
dc.identifier.pmid35406459it
dc.identifier.scopus2-s2.0-85127024311it
dc.identifier.urlhttps://dspace.unitus.it/handle/2067/48635it
dc.relation.journalCANCERSit
dc.relation.firstpage1687it
dc.relation.volume14it
dc.relation.issue7it
dc.contributor.countryITAit
dc.type.miur262*
item.fulltextWith Fulltext-
item.openairetypearticle-
item.cerifentitytypePublications-
item.grantfulltextrestricted-
item.languageiso639-1it-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.journal.journalissn2072-6694-
crisitem.journal.anceE202438-
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