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5α-Dihydrotestosterone regulates the expression of L-type calcium channels and calcium-binding protein regucalcin in human breast cancer cells with suppression of cell growth

dc.contributor.authorMarques, Ricardo
dc.contributor.authorPeres, Carina
dc.contributor.authorVaz, Cátia
dc.contributor.authorGomes, Inês
dc.contributor.authorFigueira, Marília I
dc.contributor.authorCairrão, Elisa
dc.contributor.authorVerde, Ignacio
dc.contributor.authorBaptista, Cláudio
dc.contributor.authorSocorro, Sílvia
dc.date.accessioned2019-12-04T17:24:28Z
dc.date.available2019-12-04T17:24:28Z
dc.date.issued2015-09
dc.description.abstractAndrogens have been associated with the development of normal breast, and their role in mammary gland carcinogenesis has also been described. Several studies reported that androgens inhibit breast cancer cell growth, whereas others linked their action with the modulation of calcium (Ca(2+)) pumps, Ca(2+) channels and Ca(2+)-binding proteins. Also, it is known that deregulated Ca(2+) homeostasis has been implicated in the pathophysiology of breast. The L-type Ca(2+) channels (LTCCs) were found to be up-regulated in colon, colorectal and prostate cancer, but their presence in breast tissues remains uncharacterized. On the other hand, regucalcin (RGN) is a Ca(2+)-binding protein involved in the control of mammary gland cell proliferation, which has been identified as an androgen target gene in distinct tissues except breast. This study aimed to confirm the expression and activity of LTCCs in human breast cancer cells and investigate the effect of androgens in regulating the expression of α1C subunit (Cav1.2) of LTCCs and Ca(2+)-binding protein RGN. PCR, Western blot, immunofluorescence and electrophysiological experiments demonstrated the expression and activity of Cav1.2 subunit in MCF-7 cells. The MCF-7 cells were treated with 1, 10 or 100 nM of 5α-dihydrotestosterone (DHT) for 24-72 h. The obtained results showed that 1 nM DHT up-regulated the expression of Cav1.2 subunit while diminishing RGN protein levels, which was underpinned by reduced cell viability. These findings first confirmed the presence of LTCCs in breast cancer cells and opened new perspectives for the development of therapeutic approaches targeting Ca(2+) signaling.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.doi10.1007/s12032-015-0676-xpt_PT
dc.identifier.urihttp://hdl.handle.net/10400.6/7666
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
dc.subject5α-Dihydrotestosteronept_PT
dc.subjectCav1.2pt_PT
dc.subjectDHTpt_PT
dc.subjectL-type calcium channelspt_PT
dc.subjectMCF-7 cellspt_PT
dc.subjectRegucalcinpt_PT
dc.title5α-Dihydrotestosterone regulates the expression of L-type calcium channels and calcium-binding protein regucalcin in human breast cancer cells with suppression of cell growthpt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleROLE OF REGUCALCIN IN BREAST CELLS PROLIFERATION AND TUMOR DEVELOPMENT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/5876/PEst-OE%2FSAU%2FUI0709%2F2014/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//SFRH%2FBD%2F70316%2F2010/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F66875%2F2009/PT
oaire.citation.conferencePlaceNorthwood, London, Englandpt_PT
oaire.citation.issue9pt_PT
oaire.citation.startPage228pt_PT
oaire.citation.titleMedical Oncologypt_PT
oaire.citation.volume32pt_PT
oaire.fundingStream5876
oaire.fundingStreamSFRH
person.familyNamePeres
person.familyNameVaz
person.familyNameGomes
person.familyNameFigueira
person.familyNameCairrao Rodrigues Oliveira
person.familyNameVerde
person.familyNameMaia Baptista
person.familyNameSocorro
person.givenNameCarina
person.givenNameCátia
person.givenNameInês
person.givenNameMarília
person.givenNameMaria Elisa
person.givenNameIgnacio
person.givenNameCláudio Jorge
person.givenNameSílvia Cristina da Cruz Marques
person.identifierAAB-1164-2020
person.identifierhttps://scholar.google.pt/citations?user=hFKOd_QAAAAJ&hl=pt-PT&oi=ao
person.identifierhttps://scholar.google.pt/citations?user=PA3L_h8AAAAJ&hl=pt-PT
person.identifier.ciencia-id1211-6FBA-E335
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person.identifier.ciencia-id0611-71B8-191E
person.identifier.ciencia-idD012-1D7C-791A
person.identifier.ciencia-id5115-FCBD-A31F
person.identifier.ciencia-idAB17-5C25-1F2C
person.identifier.orcid0000-0001-9399-9156
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person.identifier.orcid0000-0003-3492-5725
person.identifier.orcid0000-0002-5658-5445
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person.identifier.ridB-2669-2017
person.identifier.ridM-3991-2013
person.identifier.scopus-author-id56797773600
person.identifier.scopus-author-id55220747200
person.identifier.scopus-author-idScopus Author ID: 23476537500
person.identifier.scopus-author-id55913729400
person.identifier.scopus-author-id23097426600
person.identifier.scopus-author-id23097994600
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.embargofctCopyright cedido à editora no momento da publicação.pt_PT
rcaap.rightsclosedAccesspt_PT
rcaap.typearticlept_PT
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