CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo

Autores
Farina, Hernán Gabriel; Benavent Acero, Fernando Rodrigo; Perera, Yasser; Rodríguez, Arielis; Perea, Silvio E.; Acevedo Castro, Boris; Gomez, Roberto; Alonso, Daniel F.; Gomez, Daniel Eduardo
Año de publicación
2011
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
We have previously demonstrated that a proapoptotic cyclic peptide CIGB-300, formerly known as P15-Tat delivered into the cells by the cell-penetrating peptide Tat, was able to abrogate the CK2-mediated phosphorylation and induce tumor regression when injected directly into solid tumors in mice or by systemic administration. In this work, we studied the role of CIGB-300 on the main events that take place in angiogenesis. At non-cytotoxic doses, CIGB-300 was able to inhibit adhesion, migration, and tubular network formation induced by human umbilical vein endothelial cells (HUVEC) growing upon Matrigel in vitro. Likewise, we evaluated the cellular penetration and localization into the HUVEC cells of CIGB-300. Our results confirmed a quick cellular penetration and a cytoplasmic accumulation in the early minutes of incubation and a translocation into the nuclei beginning at 12h of treatment, with a strong presence in the perinuclear area. A microarray analysis was used to determine the genes affected by the treatment. We observed that CIGB-300 significantly decreased four genes strongly associated with tubulogenesis, growth, and differentiation of endothelial cells. The CIGB-300 was tested in vivo on chicken embryo chorioallantoic membranes (CAM), and a large number of newly formed blood vessels were significantly regressed. The results suggested that CIGB-300 has a potential as an antiangiogenic treatment. The mechanism of action may be associated with partial inhibition of VEGF and Notch pathways.
Fil: Farina, Hernán Gabriel. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Benavent Acero, Fernando Rodrigo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina
Fil: Perera, Yasser. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Rodríguez, Arielis. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Perea, Silvio E.. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Acevedo Castro, Boris. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Gomez, Roberto. No especifíca;
Fil: Alonso, Daniel F.. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina
Fil: Gomez, Daniel Eduardo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Materia
ANGIOGENESIS
CAM
CIGB-300
CK2
ENDOTHELIAL CELLS
HUVEC
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/192310
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/192310
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivoFarina, Hernán GabrielBenavent Acero, Fernando RodrigoPerera, YasserRodríguez, ArielisPerea, Silvio E.Acevedo Castro, BorisGomez, RobertoAlonso, Daniel F.Gomez, Daniel EduardoANGIOGENESISCAMCIGB-300CK2ENDOTHELIAL CELLSHUVEChttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3We have previously demonstrated that a proapoptotic cyclic peptide CIGB-300, formerly known as P15-Tat delivered into the cells by the cell-penetrating peptide Tat, was able to abrogate the CK2-mediated phosphorylation and induce tumor regression when injected directly into solid tumors in mice or by systemic administration. In this work, we studied the role of CIGB-300 on the main events that take place in angiogenesis. At non-cytotoxic doses, CIGB-300 was able to inhibit adhesion, migration, and tubular network formation induced by human umbilical vein endothelial cells (HUVEC) growing upon Matrigel in vitro. Likewise, we evaluated the cellular penetration and localization into the HUVEC cells of CIGB-300. Our results confirmed a quick cellular penetration and a cytoplasmic accumulation in the early minutes of incubation and a translocation into the nuclei beginning at 12h of treatment, with a strong presence in the perinuclear area. A microarray analysis was used to determine the genes affected by the treatment. We observed that CIGB-300 significantly decreased four genes strongly associated with tubulogenesis, growth, and differentiation of endothelial cells. The CIGB-300 was tested in vivo on chicken embryo chorioallantoic membranes (CAM), and a large number of newly formed blood vessels were significantly regressed. The results suggested that CIGB-300 has a potential as an antiangiogenic treatment. The mechanism of action may be associated with partial inhibition of VEGF and Notch pathways.Fil: Farina, Hernán Gabriel. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Benavent Acero, Fernando Rodrigo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; ArgentinaFil: Perera, Yasser. Center for Genetic Engineering and Biotechnology; CubaFil: Rodríguez, Arielis. Center for Genetic Engineering and Biotechnology; CubaFil: Perea, Silvio E.. Center for Genetic Engineering and Biotechnology; CubaFil: Acevedo Castro, Boris. Center for Genetic Engineering and Biotechnology; CubaFil: Gomez, Roberto. No especifíca;Fil: Alonso, Daniel F.. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; ArgentinaFil: Gomez, Daniel Eduardo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaElsevier Inc2011-05info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/192310Farina, Hernán Gabriel; Benavent Acero, Fernando Rodrigo; Perera, Yasser; Rodríguez, Arielis; Perea, Silvio E.; et al.; CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo; Elsevier Inc; Experimental Cell Research; 317; 12; 5-2011; 1677-16880014-4827CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0014482711001467info:eu-repo/semantics/altIdentifier/doi/10.1016/j.yexcr.2011.04.011info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-11-05T09:46:19Zoai:ri.conicet.gov.ar:11336/192310instacron: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:34982025-11-05 09:46:19.336CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
title CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
spellingShingle CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
Farina, Hernán Gabriel
ANGIOGENESIS
CAM
CIGB-300
CK2
ENDOTHELIAL CELLS
HUVEC
title_short CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
title_full CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
title_fullStr CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
title_full_unstemmed CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
title_sort CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo
dc.creator.none.fl_str_mv Farina, Hernán Gabriel
Benavent Acero, Fernando Rodrigo
Perera, Yasser
Rodríguez, Arielis
Perea, Silvio E.
Acevedo Castro, Boris
Gomez, Roberto
Alonso, Daniel F.
Gomez, Daniel Eduardo
author Farina, Hernán Gabriel
author_facet Farina, Hernán Gabriel
Benavent Acero, Fernando Rodrigo
Perera, Yasser
Rodríguez, Arielis
Perea, Silvio E.
Acevedo Castro, Boris
Gomez, Roberto
Alonso, Daniel F.
Gomez, Daniel Eduardo
author_role author
author2 Benavent Acero, Fernando Rodrigo
Perera, Yasser
Rodríguez, Arielis
Perea, Silvio E.
Acevedo Castro, Boris
Gomez, Roberto
Alonso, Daniel F.
Gomez, Daniel Eduardo
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv ANGIOGENESIS
CAM
CIGB-300
CK2
ENDOTHELIAL CELLS
HUVEC
topic ANGIOGENESIS
CAM
CIGB-300
CK2
ENDOTHELIAL CELLS
HUVEC
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv We have previously demonstrated that a proapoptotic cyclic peptide CIGB-300, formerly known as P15-Tat delivered into the cells by the cell-penetrating peptide Tat, was able to abrogate the CK2-mediated phosphorylation and induce tumor regression when injected directly into solid tumors in mice or by systemic administration. In this work, we studied the role of CIGB-300 on the main events that take place in angiogenesis. At non-cytotoxic doses, CIGB-300 was able to inhibit adhesion, migration, and tubular network formation induced by human umbilical vein endothelial cells (HUVEC) growing upon Matrigel in vitro. Likewise, we evaluated the cellular penetration and localization into the HUVEC cells of CIGB-300. Our results confirmed a quick cellular penetration and a cytoplasmic accumulation in the early minutes of incubation and a translocation into the nuclei beginning at 12h of treatment, with a strong presence in the perinuclear area. A microarray analysis was used to determine the genes affected by the treatment. We observed that CIGB-300 significantly decreased four genes strongly associated with tubulogenesis, growth, and differentiation of endothelial cells. The CIGB-300 was tested in vivo on chicken embryo chorioallantoic membranes (CAM), and a large number of newly formed blood vessels were significantly regressed. The results suggested that CIGB-300 has a potential as an antiangiogenic treatment. The mechanism of action may be associated with partial inhibition of VEGF and Notch pathways.
Fil: Farina, Hernán Gabriel. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Benavent Acero, Fernando Rodrigo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina
Fil: Perera, Yasser. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Rodríguez, Arielis. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Perea, Silvio E.. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Acevedo Castro, Boris. Center for Genetic Engineering and Biotechnology; Cuba
Fil: Gomez, Roberto. No especifíca;
Fil: Alonso, Daniel F.. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina
Fil: Gomez, Daniel Eduardo. Universidad Nacional de Quilmes. Departamento de Ciencia y Tecnología; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
description We have previously demonstrated that a proapoptotic cyclic peptide CIGB-300, formerly known as P15-Tat delivered into the cells by the cell-penetrating peptide Tat, was able to abrogate the CK2-mediated phosphorylation and induce tumor regression when injected directly into solid tumors in mice or by systemic administration. In this work, we studied the role of CIGB-300 on the main events that take place in angiogenesis. At non-cytotoxic doses, CIGB-300 was able to inhibit adhesion, migration, and tubular network formation induced by human umbilical vein endothelial cells (HUVEC) growing upon Matrigel in vitro. Likewise, we evaluated the cellular penetration and localization into the HUVEC cells of CIGB-300. Our results confirmed a quick cellular penetration and a cytoplasmic accumulation in the early minutes of incubation and a translocation into the nuclei beginning at 12h of treatment, with a strong presence in the perinuclear area. A microarray analysis was used to determine the genes affected by the treatment. We observed that CIGB-300 significantly decreased four genes strongly associated with tubulogenesis, growth, and differentiation of endothelial cells. The CIGB-300 was tested in vivo on chicken embryo chorioallantoic membranes (CAM), and a large number of newly formed blood vessels were significantly regressed. The results suggested that CIGB-300 has a potential as an antiangiogenic treatment. The mechanism of action may be associated with partial inhibition of VEGF and Notch pathways.
publishDate 2011
dc.date.none.fl_str_mv 2011-05
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/11336/192310
Farina, Hernán Gabriel; Benavent Acero, Fernando Rodrigo; Perera, Yasser; Rodríguez, Arielis; Perea, Silvio E.; et al.; CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo; Elsevier Inc; Experimental Cell Research; 317; 12; 5-2011; 1677-1688
0014-4827
CONICET Digital
CONICET
url http://hdl.handle.net/11336/192310
identifier_str_mv Farina, Hernán Gabriel; Benavent Acero, Fernando Rodrigo; Perera, Yasser; Rodríguez, Arielis; Perea, Silvio E.; et al.; CIGB-300, a proapoptotic peptide, inhibits angiogenesis in vitro and in vivo; Elsevier Inc; Experimental Cell Research; 317; 12; 5-2011; 1677-1688
0014-4827
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://www.sciencedirect.com/science/article/abs/pii/S0014482711001467
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.yexcr.2011.04.011
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier Inc
publisher.none.fl_str_mv Elsevier Inc
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
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
_version_ 1847977109765488640
score 13.087074

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