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dc.contributor.authorVillalobos Jorge, Carlos
dc.contributor.authorSobradillo Luengo, Diego
dc.contributor.authorHernández Morales, Miriam
dc.contributor.authorNúñez Llorente, Lucía 
dc.date.accessioned2021-01-15T13:53:41Z
dc.date.available2021-01-15T13:53:41Z
dc.date.issued2017
dc.identifier.citationBiochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2017, vol. 1864, n. 6. p. 843-849es
dc.identifier.issn0167-4889es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/45028
dc.descriptionProducción Científicaes
dc.description.abstractColorectal cancer (CRC) is the third most frequent form of cancer and the fourth leading cause of cancer-related death in the world. Basic and clinical data indicate that aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) may prevent colon cancer but mechanisms remain unknown. Aspirin metabolite salicylate and other NSAIDs may inhibit tumor cell growth acting on store-operated Ca2 + entry (SOCE), suggesting an important role for this pathway in CRC. Consistently, SOCE is emerging as a novel player in different forms of cancer, including CRC. SOCE and store-operated currents (SOCs) are dramatically enhanced in CRC while Ca2 + stores are partially empty in CRC cells. These features may contribute to CRC hallmarks including enhanced cell proliferation, migration, invasion and survival. At the molecular level, enhanced SOCE and depleted stores are mediated by overexpression of Orai1, Stromal interaction protein 1 (STIM1) and Transient receptor protein channel 1 (TRPC1) and downregulation of STIM2. In normal colonic cells, SOCE is mediated by Ca2 +-release activated Ca2 + channels made of STIM1, STIM2 and Orai1. In CRC cells, SOCE is mediated by different store-operated currents (SOCs) driven by STIM1, Orai1 and TRPC1. Loss of STIM2 contributes to depletion of Ca2 + stores and enhanced resistance to cell death in CRC cells. Thus, SOCE is a novel key player in CRC and inhibition by salicylate and other NSAIDs may contribute to explain chemoprevention activity.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherElsevieres
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.classificationColorectal canceres
dc.subject.classificationCáncer colorrectales
dc.subject.classificationCalciumes
dc.subject.classificationCalcioes
dc.subject.classificationAspirines
dc.subject.classificationAspirines
dc.titleCalcium remodeling in colorectal canceres
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2017 Elsevieres
dc.identifier.doi10.1016/j.bbamcr.2017.01.005es
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S0167488917300071?via%3Dihubes
dc.peerreviewedSIes
dc.description.projectMinisterio de Economía, Industria y Competitividad (grant BFU2015-70131R)es
dc.description.projectJunta de Castilla y León (grant BIO/VA46/14)es
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones


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