Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent

We have previously shown that 1α,25(OH)2-Vitamin D3 [1α,25(OH)2D3] and its less calcemic analog TX 527 inhibit the proliferation of endothelial cells transformed by the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR) and this could be partially explained by the inhibition of th...

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Autores: González Pardo, María Verónica, Suares, Alejandra Carolina, Verstuyf, Annemieke, De Clercq, Pierre, Boland, Ricardo Leopoldo, Russo, Ana Josefa
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2013
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/29860
Acceso en línea:http://hdl.handle.net/11336/29860
Access Level:acceso abierto
Palabra clave:Vitamin D
Cell Cycle
Kaposi Sarcoma
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
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network_acronym_str AR
network_name_str Argentina
repository_id_str
dc.title.none.fl_str_mv Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
title Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
spellingShingle Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
González Pardo, María Verónica
Vitamin D
Cell Cycle
Kaposi Sarcoma
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
title_short Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
title_full Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
title_fullStr Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
title_full_unstemmed Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
title_sort Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent
dc.creator.none.fl_str_mv González Pardo, María Verónica
Suares, Alejandra Carolina
Verstuyf, Annemieke
De Clercq, Pierre
Boland, Ricardo Leopoldo
Russo, Ana Josefa
author González Pardo, María Verónica
author_facet González Pardo, María Verónica
Suares, Alejandra Carolina
Verstuyf, Annemieke
De Clercq, Pierre
Boland, Ricardo Leopoldo
Russo, Ana Josefa
author_role author
author2 Suares, Alejandra Carolina
Verstuyf, Annemieke
De Clercq, Pierre
Boland, Ricardo Leopoldo
Russo, Ana Josefa
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Vitamin D
Cell Cycle
Kaposi Sarcoma
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
topic Vitamin D
Cell Cycle
Kaposi Sarcoma
https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
description We have previously shown that 1α,25(OH)2-Vitamin D3 [1α,25(OH)2D3] and its less calcemic analog TX 527 inhibit the proliferation of endothelial cells transformed by the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR) and this could be partially explained by the inhibition of the NF-κB pathway. In this work, we further explored the mechanism of action of both vitamin D compounds in Kaposi sarcoma. We investigated whether the cell cycle arrest and subsequent apoptosis of endothelial cells (SVEC) and SVEC transformed by vGPCR (SVEC-vGPCR) elicited by 1α,25(OH)2D3 and TX 527 were mediated by the vitamin D receptor (VDR). Cell cycle analysis of SVEC and SVEC-vGPCR treated with 1α,25(OH)2D3 (10 nM, 48 h) revealed that 1α,25(OH)2D3 increased the percentage of cells in the G0/G1 phase and diminished the percentage of cells in the S phase of the cell cycle. Moreover, the number of cells in the S phase was higher in SVEC-vGPCR than in SVEC due to vGPCR expression. TX 527 exerted similar effects on growth arrest in SVEC-vGPCR cells. The cell cycle changes were suppressed when the expression of the VDR was blocked by a stable transfection of shRNA against VDR. Annexin V-PI staining demonstrated apoptosis in both SVEC and SVEC-vGPCR after 1α,25(OH)2D3 and TX 527 treatment (10 nM, 24 h). Cleavage of caspase-3 detected by Western blot analysis was increased to a greater extent in SVEC than in SVEC-vGPCR cells, and this effect was also blocked in VDR knockdown cells. Altogether, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit the proliferation of SVEC and SVEC-vGPCR and induce apoptosis by a mechanism that involves the VDR.
publishDate 2013
dc.date.none.fl_str_mv 2013-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/29860
González Pardo, María Verónica; Suares, Alejandra Carolina; Verstuyf, Annemieke; De Clercq, Pierre; Boland, Ricardo Leopoldo; et al.; Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent ; Elsevier; Journal of Steroid Biochemistry and Molecular Biology; 144; Part A; 12-2013; 197-200
0960-0760
CONICET Digital
CONICET
url http://hdl.handle.net/11336/29860
identifier_str_mv González Pardo, María Verónica; Suares, Alejandra Carolina; Verstuyf, Annemieke; De Clercq, Pierre; Boland, Ricardo Leopoldo; et al.; Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent ; Elsevier; Journal of Steroid Biochemistry and Molecular Biology; 144; Part A; 12-2013; 197-200
0960-0760
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1016/j.jsbmb.2013.11.014
info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0960076013002690
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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spelling Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependentGonzález Pardo, María VerónicaSuares, Alejandra CarolinaVerstuyf, AnnemiekeDe Clercq, PierreBoland, Ricardo LeopoldoRusso, Ana JosefaVitamin DCell CycleKaposi Sarcomahttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1We have previously shown that 1α,25(OH)2-Vitamin D3 [1α,25(OH)2D3] and its less calcemic analog TX 527 inhibit the proliferation of endothelial cells transformed by the viral G protein-coupled receptor associated to Kaposi sarcoma (vGPCR) and this could be partially explained by the inhibition of the NF-κB pathway. In this work, we further explored the mechanism of action of both vitamin D compounds in Kaposi sarcoma. We investigated whether the cell cycle arrest and subsequent apoptosis of endothelial cells (SVEC) and SVEC transformed by vGPCR (SVEC-vGPCR) elicited by 1α,25(OH)2D3 and TX 527 were mediated by the vitamin D receptor (VDR). Cell cycle analysis of SVEC and SVEC-vGPCR treated with 1α,25(OH)2D3 (10 nM, 48 h) revealed that 1α,25(OH)2D3 increased the percentage of cells in the G0/G1 phase and diminished the percentage of cells in the S phase of the cell cycle. Moreover, the number of cells in the S phase was higher in SVEC-vGPCR than in SVEC due to vGPCR expression. TX 527 exerted similar effects on growth arrest in SVEC-vGPCR cells. The cell cycle changes were suppressed when the expression of the VDR was blocked by a stable transfection of shRNA against VDR. Annexin V-PI staining demonstrated apoptosis in both SVEC and SVEC-vGPCR after 1α,25(OH)2D3 and TX 527 treatment (10 nM, 24 h). Cleavage of caspase-3 detected by Western blot analysis was increased to a greater extent in SVEC than in SVEC-vGPCR cells, and this effect was also blocked in VDR knockdown cells. Altogether, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit the proliferation of SVEC and SVEC-vGPCR and induce apoptosis by a mechanism that involves the VDR.Fil: González Pardo, María Verónica. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Suares, Alejandra Carolina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Verstuyf, Annemieke. Katholikie Universiteit Leuven; BélgicaFil: De Clercq, Pierre. University of Ghent; BélgicaFil: Boland, Ricardo Leopoldo. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Russo, Ana Josefa. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaElsevier2013-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/29860González Pardo, María Verónica; Suares, Alejandra Carolina; Verstuyf, Annemieke; De Clercq, Pierre; Boland, Ricardo Leopoldo; et al.; Cell cycle arrest and apoptosis induced by 1,25(OH)2D3 and TX 527 in Kaposi sarcoma is VDR dependent ; Elsevier; Journal of Steroid Biochemistry and Molecular Biology; 144; Part A; 12-2013; 197-2000960-0760CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1016/j.jsbmb.2013.11.014info:eu-repo/semantics/altIdentifier/url/http://www.sciencedirect.com/science/article/pii/S0960076013002690info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2024-05-08T14:08:35Zoai:ri.conicet.gov.ar:11336/29860instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982024-05-08 14:08:35.727CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
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