Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells
- Autores
- Suares, Alejandra Carolina; Tapia, Cinthya Mariela; Paz, Cristina del Valle; González Pardo, María Verónica
- Año de publicación
- 2016
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- The Kaposi‘s Sarcoma-associated Herpes virus G Protein-Coupled Receptor (vGPCR) is a key molecule in the pathogenesis of Kaposi Sarcoma. In the present work, we studied the role of ERK1/2 and Akt regulation by VDR agonists, 1α,25(OH)2D3 and TX 527, of antiproliferative actions in vGPCR cells.The results showed that incubation with the MEK inhibitor PD98059 (10 µM) or Akt inhibitor, Inhibitor IV (2.5 µM) decreased cell number after 72 h treatment. Western blot analysis of time (24-48 h) and dose response studies (0.1- 100 nM) showed that 1α,25(OH)2D3 or TX527 (10 nM) decreased ERK1/2 and Akt protein phosphorylation. MKP-3, a specific phosphatase that attenuate ERK1/2 signaling, was found increased in western blot and qRT-PCR time response studies after 1α,25(OH)2D3 or TX527 treatment. This was correlated with p-ERK1/2 inhibition. ERK and Akt antineoplastic participation was evaluated using pharmacological inhibition. qRT-PCR studies (24h) revealed that 1α,25(OH)2D3, TX 527 (both 10nM) and PD (10 μM) treatment decreased IL-6, A20 and NF-κB gene expression while the opposite effect was observed for Bim. However, all genes studied exhibited an mRNA increased in cells incubated with Inhibitor IV (2.5 μM). All together, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit proliferation involving ERK and Akt inhibition as part of an anti-angiogenic and anti-inflammatory mechanism^.
Fil: Suares, Alejandra Carolina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Tapia, Cinthya Mariela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
Fil: Paz, Cristina del Valle. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina
Fil: González Pardo, María Verónica. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina
LII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular
Córdoba
Argentina
Sociedad Argentina de Investigación en Bioquímica y Biología Molecular - Materia
-
VITAMIN D
TX 527
KAPOSI SARCOMA
ANTINEOPLASTIC - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
.jpg)
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/235549
Ver los metadatos del registro completo
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Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cellsSuares, Alejandra CarolinaTapia, Cinthya MarielaPaz, Cristina del ValleGonzález Pardo, María VerónicaVITAMIN DTX 527KAPOSI SARCOMAANTINEOPLASTIChttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The Kaposi‘s Sarcoma-associated Herpes virus G Protein-Coupled Receptor (vGPCR) is a key molecule in the pathogenesis of Kaposi Sarcoma. In the present work, we studied the role of ERK1/2 and Akt regulation by VDR agonists, 1α,25(OH)2D3 and TX 527, of antiproliferative actions in vGPCR cells.The results showed that incubation with the MEK inhibitor PD98059 (10 µM) or Akt inhibitor, Inhibitor IV (2.5 µM) decreased cell number after 72 h treatment. Western blot analysis of time (24-48 h) and dose response studies (0.1- 100 nM) showed that 1α,25(OH)2D3 or TX527 (10 nM) decreased ERK1/2 and Akt protein phosphorylation. MKP-3, a specific phosphatase that attenuate ERK1/2 signaling, was found increased in western blot and qRT-PCR time response studies after 1α,25(OH)2D3 or TX527 treatment. This was correlated with p-ERK1/2 inhibition. ERK and Akt antineoplastic participation was evaluated using pharmacological inhibition. qRT-PCR studies (24h) revealed that 1α,25(OH)2D3, TX 527 (both 10nM) and PD (10 μM) treatment decreased IL-6, A20 and NF-κB gene expression while the opposite effect was observed for Bim. However, all genes studied exhibited an mRNA increased in cells incubated with Inhibitor IV (2.5 μM). All together, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit proliferation involving ERK and Akt inhibition as part of an anti-angiogenic and anti-inflammatory mechanism^.Fil: Suares, Alejandra Carolina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Tapia, Cinthya Mariela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaFil: Paz, Cristina del Valle. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; ArgentinaFil: González Pardo, María Verónica. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; ArgentinaLII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología MolecularCórdobaArgentinaSociedad Argentina de Investigación en Bioquímica y Biología MolecularTech Science Press2016info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/235549Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells; LII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Córdoba; Argentina; 2016; 1-3CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://newsite.saib.org.ar/publicaciones/Nacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:51:46Zoai:ri.conicet.gov.ar:11336/235549instacron: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:34982025-09-03 09:51:46.508CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| title |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| spellingShingle |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells Suares, Alejandra Carolina VITAMIN D TX 527 KAPOSI SARCOMA ANTINEOPLASTIC |
| title_short |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| title_full |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| title_fullStr |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| title_full_unstemmed |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| title_sort |
Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells |
| dc.creator.none.fl_str_mv |
Suares, Alejandra Carolina Tapia, Cinthya Mariela Paz, Cristina del Valle González Pardo, María Verónica |
| author |
Suares, Alejandra Carolina |
| author_facet |
Suares, Alejandra Carolina Tapia, Cinthya Mariela Paz, Cristina del Valle González Pardo, María Verónica |
| author_role |
author |
| author2 |
Tapia, Cinthya Mariela Paz, Cristina del Valle González Pardo, María Verónica |
| author2_role |
author author author |
| dc.subject.none.fl_str_mv |
VITAMIN D TX 527 KAPOSI SARCOMA ANTINEOPLASTIC |
| topic |
VITAMIN D TX 527 KAPOSI SARCOMA ANTINEOPLASTIC |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
The Kaposi‘s Sarcoma-associated Herpes virus G Protein-Coupled Receptor (vGPCR) is a key molecule in the pathogenesis of Kaposi Sarcoma. In the present work, we studied the role of ERK1/2 and Akt regulation by VDR agonists, 1α,25(OH)2D3 and TX 527, of antiproliferative actions in vGPCR cells.The results showed that incubation with the MEK inhibitor PD98059 (10 µM) or Akt inhibitor, Inhibitor IV (2.5 µM) decreased cell number after 72 h treatment. Western blot analysis of time (24-48 h) and dose response studies (0.1- 100 nM) showed that 1α,25(OH)2D3 or TX527 (10 nM) decreased ERK1/2 and Akt protein phosphorylation. MKP-3, a specific phosphatase that attenuate ERK1/2 signaling, was found increased in western blot and qRT-PCR time response studies after 1α,25(OH)2D3 or TX527 treatment. This was correlated with p-ERK1/2 inhibition. ERK and Akt antineoplastic participation was evaluated using pharmacological inhibition. qRT-PCR studies (24h) revealed that 1α,25(OH)2D3, TX 527 (both 10nM) and PD (10 μM) treatment decreased IL-6, A20 and NF-κB gene expression while the opposite effect was observed for Bim. However, all genes studied exhibited an mRNA increased in cells incubated with Inhibitor IV (2.5 μM). All together, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit proliferation involving ERK and Akt inhibition as part of an anti-angiogenic and anti-inflammatory mechanism^. Fil: Suares, Alejandra Carolina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina Fil: Tapia, Cinthya Mariela. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina Fil: Paz, Cristina del Valle. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Biomédicas; Argentina Fil: González Pardo, María Verónica. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Ciencias Biológicas y Biomédicas del Sur. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia. Instituto de Ciencias Biológicas y Biomédicas del Sur; Argentina LII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular Córdoba Argentina Sociedad Argentina de Investigación en Bioquímica y Biología Molecular |
| description |
The Kaposi‘s Sarcoma-associated Herpes virus G Protein-Coupled Receptor (vGPCR) is a key molecule in the pathogenesis of Kaposi Sarcoma. In the present work, we studied the role of ERK1/2 and Akt regulation by VDR agonists, 1α,25(OH)2D3 and TX 527, of antiproliferative actions in vGPCR cells.The results showed that incubation with the MEK inhibitor PD98059 (10 µM) or Akt inhibitor, Inhibitor IV (2.5 µM) decreased cell number after 72 h treatment. Western blot analysis of time (24-48 h) and dose response studies (0.1- 100 nM) showed that 1α,25(OH)2D3 or TX527 (10 nM) decreased ERK1/2 and Akt protein phosphorylation. MKP-3, a specific phosphatase that attenuate ERK1/2 signaling, was found increased in western blot and qRT-PCR time response studies after 1α,25(OH)2D3 or TX527 treatment. This was correlated with p-ERK1/2 inhibition. ERK and Akt antineoplastic participation was evaluated using pharmacological inhibition. qRT-PCR studies (24h) revealed that 1α,25(OH)2D3, TX 527 (both 10nM) and PD (10 μM) treatment decreased IL-6, A20 and NF-κB gene expression while the opposite effect was observed for Bim. However, all genes studied exhibited an mRNA increased in cells incubated with Inhibitor IV (2.5 μM). All together, these results suggest that 1α,25(OH)2D3 and TX 527 inhibit proliferation involving ERK and Akt inhibition as part of an anti-angiogenic and anti-inflammatory mechanism^. |
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2016 |
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2016 |
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Antineoplastic effect of ERK 1/2 and Akt inhibition by VDR agonists in vGPCR endothelial cells; LII Reunión Anual Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; Córdoba; Argentina; 2016; 1-3 CONICET Digital CONICET |
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