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β-Adrenoceptor Activation in Breast MCF-10A Cells Induces a Pattern of Catecholamine Production Similar to that of Tumorigenic MCF-7 Cells

dc.contributor.authorAmaro, Filipa
dc.contributor.authorSilva, Dany
dc.contributor.authorReguengo, Henrique
dc.contributor.authorOliveira, José Carlos
dc.contributor.authorQuintas, Clara
dc.contributor.authorVale, Nuno
dc.contributor.authorGonçalves, Jorge
dc.contributor.authorFresco, Paula
dc.date.accessioned2021-12-09T15:09:56Z
dc.date.available2021-12-09T15:09:56Z
dc.date.issued2020-10-27
dc.description.abstractAdrenaline, which participates in the neuroendocrine response that occurs during stress and perimenopause, may be tumorigenic. This exploratory study aimed at investigating whether non-tumorigenic and tumorigenic human breast epithelial cell lines are able to synthesize adrenaline. The study was carried out in non-tumorigenic (MCF-10A) and tumorigenic (MCF-7) human breast cell lines. Expression of enzymes involved in adrenaline synthesis was characterized by RT-qPCR, immunocytochemistry and western blot. Catecholamines and analogue compounds were quantified by HPLC-ECD. Functional assessment of the impact of drugs on cells' tumorigenic potential was assessed by determination of cell viability and clonogenic ability. Both MCF-10A and MCF-7 cells produce catecholamines, but the capacity to produce adrenaline is lower in MCF-10A cells. β-adrenoceptor activation increases the capacity of MCF-10A cells to produce adrenaline and favor both cell viability and colony formation. It is concluded that exposure of human breast epithelial cells to β-adrenoceptor agonists increases cell proliferation and the capacity to produce adrenaline, creating an autocrine potential to spread these adrenergic effects in a feed-forward loop. It is conceivable that these effects are related to tumorigenesis, bringing a new perspective to understand the claimed anticancer effects of propranolol and the increase in breast cancer incidence caused by stress or during perimenopause.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationAmaro F, Silva D, Reguengo H, et al. β-Adrenoceptor Activation in Breast MCF-10A Cells Induces a Pattern of Catecholamine Production Similar to that of Tumorigenic MCF-7 Cells. Int J Mol Sci. 2020;21(21):7968. doi:10.3390/ijms21217968pt_PT
dc.identifier.doi10.3390/ijms21217968pt_PT
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/10400.16/2649
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherMDPIpt_PT
dc.relation.publisherversionhttps://www.mdpi.com/1422-0067/21/21/7968pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectbreast cancerpt_PT
dc.subjectcatecholamine synthesispt_PT
dc.subjectpropranololpt_PT
dc.subjecttumorigenic processpt_PT
dc.subjectβ-adrenoceptorspt_PT
dc.titleβ-Adrenoceptor Activation in Breast MCF-10A Cells Induces a Pattern of Catecholamine Production Similar to that of Tumorigenic MCF-7 Cellspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.conferencePlaceSwitzerlandpt_PT
oaire.citation.issue21pt_PT
oaire.citation.startPage7968pt_PT
oaire.citation.titleInternational Journal of Molecular Sciencespt_PT
oaire.citation.volume21pt_PT
person.familyNameReguengo Luz
person.familyNameOliveira
person.givenNameHenrique
person.givenNameJosé Carlos
person.identifier806053
person.identifier.ciencia-idD315-6421-A327
person.identifier.ciencia-id801F-D4FE-8694
person.identifier.orcid0000-0002-0246-6790
person.identifier.orcid0000-0003-2142-6839
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationdc00d9fd-3fff-4a83-a190-d0111a136116
relation.isAuthorOfPublicationbd6d8008-2622-4368-8ded-4ec1c1160c82
relation.isAuthorOfPublication.latestForDiscoverybd6d8008-2622-4368-8ded-4ec1c1160c82

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