Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression
- Autores
- Principe, Gabriel; Lezcano, Virginia Alicia; Tiburzi, Silvina Mabel; Miravalles, Alicia Beatriz; Maniscalchi, Athina del Valle; Salvador, Gabriela Alejandra; González Pardo, María Verónica
- Año de publicación
- 2024
- Idioma
- inglés
- Tipo de recurso
- documento de conferencia
- Estado
- versión publicada
- Descripción
- Quercetin (QUE) is a natural flavonoid classified as a phytoestrogen due to its resemblance with human estrogens. Although its anticancer properties are well-known in various cancer models, its effect on viral-induced cancers has been less studied. Kaposi’s sarcoma (KS) is a virally induced cancer caused by Kaposi’s sarcoma-associated herpesvirus, which contains a constitutively activated viral G protein-coupled receptor (vGPCR) expressed during the viral lytic phase, leading to oncogenesis and angiogenesis through the activation of several signaling pathways. Our previous studies indicated that QUE inhibits vGPCR-mediated cell proliferation in vitro and tumor growth in vivo. In this work, we investigated the mechanism by which QUE exerts its antitumoral effects. QUE treatment (30 μM) for 24 h induced marked morphological changes in vGPCR cells consistent with apoptosis, including cell shrinkage and the formation of apoptotic bodies, as observed by scanning electron microscopy. In parallel experiments, a highly significant increase in cleaved caspase-3 protein levels was detected by Western blot analysis, further confirming apoptotic induction. To investigate oxidative stress, vGPCR cells were treated with QUE (5-45 μM) for 24 h or hydrogen peroxide (0.5 mM, 45 min) as a positive control, and intracellular oxidant levels were measured using the fluorogenic probe 2′,7′-dichlorofluorescin diacetate. QUE treatment led to a concentration-dependent increase in oxidant levels. Additionally, lipid peroxidation levels, evaluated by TBARS assay, were significantly increased by QUE (30 μM). Moreover, comet assay analysis of vGPCR cells treated with QUE (30 μM) for 48 h indicated a significant increase in DNA damage, evidenced by longer comet tails. Further exploration of signaling pathways by Western blot revealed that QUE (10-50 μM) for 48h increased p38 and ERK1/2 phosphorylation, whereas AKT phosphorylation remained unchanged. In conclusion, our findings suggest that QUE-induced oxidative stress and DNA damage may lead to apoptosis, with concurrent activation of stress-responsive signaling pathways (p38 and ERK1/2) potentially serving as adaptive responses to mitigate QUE’s cytotoxic effects
Fil: Principe, Gabriel. 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: Lezcano, Virginia Alicia. 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: Tiburzi, Silvina Mabel. 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: Miravalles, Alicia Beatriz. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: Maniscalchi, Athina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina
Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina
Fil: González Pardo, María Verónica. 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
LX Reunión Anual de Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular
Cordoba
Argentina
Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular - Materia
-
QUERCETIN
G PROTEIN-COUPLED RECEPTOR
ENDOTHELIAL CELLS
KAPOSI - 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:11336/260335
Ver los metadatos del registro completo
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Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expressionPrincipe, GabrielLezcano, Virginia AliciaTiburzi, Silvina MabelMiravalles, Alicia BeatrizManiscalchi, Athina del ValleSalvador, Gabriela AlejandraGonzález Pardo, María VerónicaQUERCETING PROTEIN-COUPLED RECEPTORENDOTHELIAL CELLSKAPOSIhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Quercetin (QUE) is a natural flavonoid classified as a phytoestrogen due to its resemblance with human estrogens. Although its anticancer properties are well-known in various cancer models, its effect on viral-induced cancers has been less studied. Kaposi’s sarcoma (KS) is a virally induced cancer caused by Kaposi’s sarcoma-associated herpesvirus, which contains a constitutively activated viral G protein-coupled receptor (vGPCR) expressed during the viral lytic phase, leading to oncogenesis and angiogenesis through the activation of several signaling pathways. Our previous studies indicated that QUE inhibits vGPCR-mediated cell proliferation in vitro and tumor growth in vivo. In this work, we investigated the mechanism by which QUE exerts its antitumoral effects. QUE treatment (30 μM) for 24 h induced marked morphological changes in vGPCR cells consistent with apoptosis, including cell shrinkage and the formation of apoptotic bodies, as observed by scanning electron microscopy. In parallel experiments, a highly significant increase in cleaved caspase-3 protein levels was detected by Western blot analysis, further confirming apoptotic induction. To investigate oxidative stress, vGPCR cells were treated with QUE (5-45 μM) for 24 h or hydrogen peroxide (0.5 mM, 45 min) as a positive control, and intracellular oxidant levels were measured using the fluorogenic probe 2′,7′-dichlorofluorescin diacetate. QUE treatment led to a concentration-dependent increase in oxidant levels. Additionally, lipid peroxidation levels, evaluated by TBARS assay, were significantly increased by QUE (30 μM). Moreover, comet assay analysis of vGPCR cells treated with QUE (30 μM) for 48 h indicated a significant increase in DNA damage, evidenced by longer comet tails. Further exploration of signaling pathways by Western blot revealed that QUE (10-50 μM) for 48h increased p38 and ERK1/2 phosphorylation, whereas AKT phosphorylation remained unchanged. In conclusion, our findings suggest that QUE-induced oxidative stress and DNA damage may lead to apoptosis, with concurrent activation of stress-responsive signaling pathways (p38 and ERK1/2) potentially serving as adaptive responses to mitigate QUE’s cytotoxic effectsFil: Principe, Gabriel. 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: Lezcano, Virginia Alicia. 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: Tiburzi, Silvina Mabel. 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: Miravalles, Alicia Beatriz. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Maniscalchi, Athina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; ArgentinaFil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: González Pardo, María Verónica. 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; ArgentinaLX Reunión Anual de Sociedad Argentina de Investigaciones en Bioquímica y Biología MolecularCordobaArgentinaSociedad Argentina de Investigaciones en Bioquímica y Biología MolecularSociedad Argentina de Investigaciones en Bioquímica y Biología Molecular2024info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectCongresoBookhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/260335Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression; LX Reunión Anual de Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; Cordoba; Argentina; 2024; 130-131CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://saib.org.ar/congreso-2024/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 Técnicas2025-09-03T10:08:28Zoai:ri.conicet.gov.ar:11336/260335instacron: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 10:08:28.611CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
| dc.title.none.fl_str_mv |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| title |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| spellingShingle |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression Principe, Gabriel QUERCETIN G PROTEIN-COUPLED RECEPTOR ENDOTHELIAL CELLS KAPOSI |
| title_short |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| title_full |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| title_fullStr |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| title_full_unstemmed |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| title_sort |
Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression |
| dc.creator.none.fl_str_mv |
Principe, Gabriel Lezcano, Virginia Alicia Tiburzi, Silvina Mabel Miravalles, Alicia Beatriz Maniscalchi, Athina del Valle Salvador, Gabriela Alejandra González Pardo, María Verónica |
| author |
Principe, Gabriel |
| author_facet |
Principe, Gabriel Lezcano, Virginia Alicia Tiburzi, Silvina Mabel Miravalles, Alicia Beatriz Maniscalchi, Athina del Valle Salvador, Gabriela Alejandra González Pardo, María Verónica |
| author_role |
author |
| author2 |
Lezcano, Virginia Alicia Tiburzi, Silvina Mabel Miravalles, Alicia Beatriz Maniscalchi, Athina del Valle Salvador, Gabriela Alejandra González Pardo, María Verónica |
| author2_role |
author author author author author author |
| dc.subject.none.fl_str_mv |
QUERCETIN G PROTEIN-COUPLED RECEPTOR ENDOTHELIAL CELLS KAPOSI |
| topic |
QUERCETIN G PROTEIN-COUPLED RECEPTOR ENDOTHELIAL CELLS KAPOSI |
| purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
| dc.description.none.fl_txt_mv |
Quercetin (QUE) is a natural flavonoid classified as a phytoestrogen due to its resemblance with human estrogens. Although its anticancer properties are well-known in various cancer models, its effect on viral-induced cancers has been less studied. Kaposi’s sarcoma (KS) is a virally induced cancer caused by Kaposi’s sarcoma-associated herpesvirus, which contains a constitutively activated viral G protein-coupled receptor (vGPCR) expressed during the viral lytic phase, leading to oncogenesis and angiogenesis through the activation of several signaling pathways. Our previous studies indicated that QUE inhibits vGPCR-mediated cell proliferation in vitro and tumor growth in vivo. In this work, we investigated the mechanism by which QUE exerts its antitumoral effects. QUE treatment (30 μM) for 24 h induced marked morphological changes in vGPCR cells consistent with apoptosis, including cell shrinkage and the formation of apoptotic bodies, as observed by scanning electron microscopy. In parallel experiments, a highly significant increase in cleaved caspase-3 protein levels was detected by Western blot analysis, further confirming apoptotic induction. To investigate oxidative stress, vGPCR cells were treated with QUE (5-45 μM) for 24 h or hydrogen peroxide (0.5 mM, 45 min) as a positive control, and intracellular oxidant levels were measured using the fluorogenic probe 2′,7′-dichlorofluorescin diacetate. QUE treatment led to a concentration-dependent increase in oxidant levels. Additionally, lipid peroxidation levels, evaluated by TBARS assay, were significantly increased by QUE (30 μM). Moreover, comet assay analysis of vGPCR cells treated with QUE (30 μM) for 48 h indicated a significant increase in DNA damage, evidenced by longer comet tails. Further exploration of signaling pathways by Western blot revealed that QUE (10-50 μM) for 48h increased p38 and ERK1/2 phosphorylation, whereas AKT phosphorylation remained unchanged. In conclusion, our findings suggest that QUE-induced oxidative stress and DNA damage may lead to apoptosis, with concurrent activation of stress-responsive signaling pathways (p38 and ERK1/2) potentially serving as adaptive responses to mitigate QUE’s cytotoxic effects Fil: Principe, Gabriel. 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: Lezcano, Virginia Alicia. 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: Tiburzi, Silvina Mabel. 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: Miravalles, Alicia Beatriz. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina Fil: Maniscalchi, Athina del Valle. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina Fil: Salvador, Gabriela Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; Argentina Fil: González Pardo, María Verónica. 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 LX Reunión Anual de Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular Cordoba Argentina Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular |
| description |
Quercetin (QUE) is a natural flavonoid classified as a phytoestrogen due to its resemblance with human estrogens. Although its anticancer properties are well-known in various cancer models, its effect on viral-induced cancers has been less studied. Kaposi’s sarcoma (KS) is a virally induced cancer caused by Kaposi’s sarcoma-associated herpesvirus, which contains a constitutively activated viral G protein-coupled receptor (vGPCR) expressed during the viral lytic phase, leading to oncogenesis and angiogenesis through the activation of several signaling pathways. Our previous studies indicated that QUE inhibits vGPCR-mediated cell proliferation in vitro and tumor growth in vivo. In this work, we investigated the mechanism by which QUE exerts its antitumoral effects. QUE treatment (30 μM) for 24 h induced marked morphological changes in vGPCR cells consistent with apoptosis, including cell shrinkage and the formation of apoptotic bodies, as observed by scanning electron microscopy. In parallel experiments, a highly significant increase in cleaved caspase-3 protein levels was detected by Western blot analysis, further confirming apoptotic induction. To investigate oxidative stress, vGPCR cells were treated with QUE (5-45 μM) for 24 h or hydrogen peroxide (0.5 mM, 45 min) as a positive control, and intracellular oxidant levels were measured using the fluorogenic probe 2′,7′-dichlorofluorescin diacetate. QUE treatment led to a concentration-dependent increase in oxidant levels. Additionally, lipid peroxidation levels, evaluated by TBARS assay, were significantly increased by QUE (30 μM). Moreover, comet assay analysis of vGPCR cells treated with QUE (30 μM) for 48 h indicated a significant increase in DNA damage, evidenced by longer comet tails. Further exploration of signaling pathways by Western blot revealed that QUE (10-50 μM) for 48h increased p38 and ERK1/2 phosphorylation, whereas AKT phosphorylation remained unchanged. In conclusion, our findings suggest that QUE-induced oxidative stress and DNA damage may lead to apoptosis, with concurrent activation of stress-responsive signaling pathways (p38 and ERK1/2) potentially serving as adaptive responses to mitigate QUE’s cytotoxic effects |
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2024 |
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Deciphering the mechanism of quercetin-Induced cell death in endothelial cells transformed by viral G protein-coupled receptor expression; LX Reunión Anual de Sociedad Argentina de Investigaciones en Bioquímica y Biología Molecular; Cordoba; Argentina; 2024; 130-131 CONICET Digital CONICET |
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