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Downregulated Regucalcin Expression Induces a Cancer-like Phenotype in Non-Neoplastic Prostate Cells and Augments the Aggressiveness of Prostate Cancer Cells: Interplay with the G Protein-Coupled Oestrogen Receptor?

2024-11-24Journal article Open access
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dc.contributor.authorFonseca, Lara R. S.
dc.contributor.authorCarreira, Ricardo J. P.
dc.contributor.authorFeijó, Mariana
dc.contributor.authorCavaco, J. E.
dc.contributor.authorCardoso, Henrique
dc.contributor.authorVaz, C. V.
dc.contributor.authorFigueira, Marília I.
dc.contributor.authorSocorro, Sílvia
dc.date.accessioned2025-02-24T14:44:00Z
dc.date.available2025-02-24T14:44:00Z
dc.date.issued2024-11-24
dc.description.abstractBackground/objectives: Regucalcin (RGN) is a calcium-binding protein and an oestrogen target gene, which has been shown to play essential roles beyond calcium homeostasis. Decreased RGN expression was identified in several cancers, including prostate cancer (PCa). However, it is unknown if the loss of RGN is a cause or a consequence of malignancy. Also, it needs confirmation if RGN oestrogenic regulation occurs through the G-protein-coupled oestrogen receptor (GPER). This study investigates how RGN knockdown affects prostate cell fate and metabolism and highlights the GPER/RGN interplay in PCa. Methods: Bioinformatic analysis assessed the relationship between RGN expression levels and patients' outcomes. RGN knockdown (siRNA) was performed in non-neoplastic prostate and castration-resistant PCa. Wild-type and RGN knockdown PCa cells were treated with the GPER agonist G1. Viability (MTT), proliferation (Ki-67 immunocytochemistry), apoptosis (caspase-3-like activity) and migration (Transwell assays) were evaluated. Spectrophotometric analysis was used to determine glucose consumption, lactate production and lactate dehydrogenase activity. Lipid content was assessed using the Oil Red assay. Results/conclusions: Bioinformatic analysis showed that the loss of RGN correlates with the development of metastatic PCa and poor survival outcomes. RGN knockdown induced a cancer-like phenotype in PNT1A cells, indicated by increased cell viability and proliferation and reduced apoptosis. In DU145 PCa cells, RGN knockdown augmented migration and enhanced the glycolytic profile, which indicates increased aggressiveness, in line with patients' data. GPER activation modulated RGN expression in PCa cells and RGN knockdown in DU145 cells influenced GPER actions, which highlighted an interplay between these molecular players with relevance for their potential use as biomarkers or therapeutic targets.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationFonseca, L.R.S.; Carreira, R.J.P.; Feijó, M.; Cavaco, J.E.B.; Cardoso, H.J.; Vaz, C.V.; Figueira, M.I.; Socorro, S. Downregulated Regucalcin Expression Induces a Cancer-like Phenotype in Non-Neoplastic Prostate Cells and Augments the Aggressiveness of Prostate Cancer Cells: Interplay with the G Protein-Coupled Oestrogen Receptor? Cancers 2024, 16, 3932. https:// doi.org/10.3390/cancers16233932pt_PT
dc.identifier.doi10.3390/cancers16233932pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.6/15123
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherAcademic Editor: Aria Baniahmadpt_PT
dc.relationHealth Sciences Research Centre
dc.relationObesogens-induced deregulation of periprostatic adipose tissue: a driven force in the onset and progression of prostate cancer
dc.relationPortuguese Platform of BioImaging
dc.relation.publisherversionhttps://www.mdpi.com/2072-6694/16/23/3932pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectG-protein-coupled oestrogen receptorpt_PT
dc.subjectMetabolismpt_PT
dc.subjectMetastisationpt_PT
dc.subjectProstate cancerpt_PT
dc.subjectRegucalcinpt_PT
dc.subjectSurvivalpt_PT
dc.titleDownregulated Regucalcin Expression Induces a Cancer-like Phenotype in Non-Neoplastic Prostate Cells and Augments the Aggressiveness of Prostate Cancer Cells: Interplay with the G Protein-Coupled Oestrogen Receptor?pt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleHealth Sciences Research Centre
oaire.awardTitleObesogens-induced deregulation of periprostatic adipose tissue: a driven force in the onset and progression of prostate cancer
oaire.awardTitlePortuguese Platform of BioImaging
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UID%2FMulti%2F00709%2F2019/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/POR_CENTRO/2021.07634.BD/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//2021.07367.BD/PT
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/9444 - RNIIIE/PINFRA%2F22122%2F2016/PT
oaire.citation.issue23pt_PT
oaire.citation.startPage3932pt_PT
oaire.citation.titleCancerspt_PT
oaire.citation.volume16pt_PT
oaire.fundingStream6817 - DCRRNI ID
oaire.fundingStreamPOR_CENTRO
oaire.fundingStream9444 - RNIIIE
person.familyNameFonseca
person.familyNamePereira Carreira
person.familyNamePombal Feijó
person.familyNameCavaco
person.familyNameCardoso
person.familyNameVaz
person.familyNameFigueira
person.familyNameSocorro
person.givenNameLara R. S.
person.givenNameRicardo João
person.givenNameMariana
person.givenNameJose Eduardo
person.givenNameHenrique
person.givenNameCátia
person.givenNameMarília
person.givenNameSílvia Cristina da Cruz Marques
person.identifierhttps://scholar.google.pt/citations?user=PA3L_h8AAAAJ&hl=pt-PT
person.identifier.ciencia-id1618-46EE-4DA4
person.identifier.ciencia-id1512-79F7-B39A
person.identifier.ciencia-idFC1F-F519-8104
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person.identifier.ciencia-id1C1D-F91F-D937
person.identifier.ciencia-id881D-B823-72F5
person.identifier.ciencia-idAB17-5C25-1F2C
person.identifier.orcid0000-0002-8789-4048
person.identifier.orcid0000-0002-5330-5276
person.identifier.orcid0000-0002-3879-733X
person.identifier.orcid0000-0002-5750-2875
person.identifier.orcid0000-0002-7720-4234
person.identifier.orcid0000-0003-0901-9931
person.identifier.orcid0000-0001-8181-488X
person.identifier.ridN-7461-2013
person.identifier.scopus-author-id6603341330
person.identifier.scopus-author-id56421799300
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.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
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
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