Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate...

Autores
Cardenas, Sofía; Colombero, Cecilia; Panelo, Laura Carolina; Dakarapu, Rambabu; Falck, John; Costas, Monica Alejandra; Nowicki, Susana
Año de publicación
2019
Idioma
español castellano
Tipo de recurso
documento de conferencia
Estado
versión publicada
Descripción
20-HETE, the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to identify intracellular signaling molecules activated upon GPR75 stimulation by 20-HETE in PC-3 cells.Cells were incubated with 20-HETE (0.1 nM) in the presence or absence of the antagonist of the 20-HETE receptor, AAA (5 or 10 uM). Protein expression of the inducible focal adhesion protein Hydrogen Peroxide Inducible Clone-5 (HIC-5), the phosphorylated and total form of NF-kB, AKT, p38 MAP-Kinase (p38) and EGFR were assessed by western blot. Intracellular localization of p-AKT, NF-kB and PKCa were determined by immunofluorescence and subcellular fractionation. Migration of PC-3 cells incubated with diferentes inhibitors were evaluated by scratch wound healing assay. Results were analyzed using one-way ANOVA followed by Dunnet?s.Incubation with 20-HETE (2 h) increased the phosphorylation of EGFR, NF-kB and AKT by 146, 172 and 219%, respectively (vs control, p<0.01 for NF-kB, and p<0.001 for EGFR and AKT, n=3), and this was inhibited by AAA (vs 20-HETE alone, p<0.05 for NF-kB, p<0.01 for AKT and p<0.001 for EGFR). AAA alone increased p-38 phosphorylation by 248% (p<0.001 vs control, n=3). 20-HETE (1 h) induced the translocation of p-AKT to the nuclei (p<0.001, n=3) and promoted the redistribution of PKCa out of the nuclei (p<0.05, n=3) to the plasma membrane (p<0.001). Both effects were inhibited by AAA (vs 20-HETE, p<0.01 for AKT and p<0.05 for PKCa). AAA alone reduced the nuclear signal of p-AKT and NF-kB usually activated in tumoral cells (p<0.001 for both, n=3). Additionally, 20-HETE (12 h) increased by 150% the protein expression of Hic-5 (p<0.0001, n=5) and this was abolished by AAA (p<0.001).Our results show that 20-HETE modulates signaling pathways known to be deregulated in malignant cells through the GPR75-axis.
Fil: Cardenas, Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Fil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Fil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados Unidos
Fil: Falck, John. University of Texas. Southwestern Medical Center; Estados Unidos
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Reunión anual de las Sociedades de Biociencia
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Asociación Argentina de Farmacología Experimental
Sociedad Argentina de Biología
Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio
Sociedad Argentina de Protozoología
Materia
CANCER DE PROSTATA
EICOSANOIDES
SEÑALES INTRACELULARES
RECEPTOR GPR75
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:11336/154163
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cellsCardenas, SofíaColombero, CeciliaPanelo, Laura CarolinaDakarapu, RambabuFalck, JohnCostas, Monica AlejandraNowicki, SusanaCANCER DE PROSTATAEICOSANOIDESSEÑALES INTRACELULARESRECEPTOR GPR75https://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/320-HETE, the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to identify intracellular signaling molecules activated upon GPR75 stimulation by 20-HETE in PC-3 cells.Cells were incubated with 20-HETE (0.1 nM) in the presence or absence of the antagonist of the 20-HETE receptor, AAA (5 or 10 uM). Protein expression of the inducible focal adhesion protein Hydrogen Peroxide Inducible Clone-5 (HIC-5), the phosphorylated and total form of NF-kB, AKT, p38 MAP-Kinase (p38) and EGFR were assessed by western blot. Intracellular localization of p-AKT, NF-kB and PKCa were determined by immunofluorescence and subcellular fractionation. Migration of PC-3 cells incubated with diferentes inhibitors were evaluated by scratch wound healing assay. Results were analyzed using one-way ANOVA followed by Dunnet?s.Incubation with 20-HETE (2 h) increased the phosphorylation of EGFR, NF-kB and AKT by 146, 172 and 219%, respectively (vs control, p<0.01 for NF-kB, and p<0.001 for EGFR and AKT, n=3), and this was inhibited by AAA (vs 20-HETE alone, p<0.05 for NF-kB, p<0.01 for AKT and p<0.001 for EGFR). AAA alone increased p-38 phosphorylation by 248% (p<0.001 vs control, n=3). 20-HETE (1 h) induced the translocation of p-AKT to the nuclei (p<0.001, n=3) and promoted the redistribution of PKCa out of the nuclei (p<0.05, n=3) to the plasma membrane (p<0.001). Both effects were inhibited by AAA (vs 20-HETE, p<0.01 for AKT and p<0.05 for PKCa). AAA alone reduced the nuclear signal of p-AKT and NF-kB usually activated in tumoral cells (p<0.001 for both, n=3). Additionally, 20-HETE (12 h) increased by 150% the protein expression of Hic-5 (p<0.0001, n=5) and this was abolished by AAA (p<0.001).Our results show that 20-HETE modulates signaling pathways known to be deregulated in malignant cells through the GPR75-axis.Fil: Cardenas, Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaFil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados UnidosFil: Falck, John. University of Texas. Southwestern Medical Center; Estados UnidosFil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; ArgentinaFil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; ArgentinaReunión anual de las Sociedades de BiocienciaMar del PlataArgentinaSociedad Argentina de Investigación ClínicaAsociación Argentina de Farmacología ExperimentalSociedad Argentina de BiologíaAsociación Argentina de Ciencia y Tecnología de Animales de LaboratorioSociedad Argentina de ProtozoologíaFundación Revista Medicina2019info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/conferenceObjectReuniónJournalhttp://purl.org/coar/resource_type/c_5794info:ar-repo/semantics/documentoDeConferenciaapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/154163Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells; Reunión anual de las Sociedades de Biociencia; Mar del Plata; Argentina; 2019; 82-820025-76801669-9106CONICET DigitalCONICETspainfo:eu-repo/semantics/altIdentifier/url/https://medicinabuenosaires.com/revistas/vol79-19/s4/vol79_s4.pdfNacionalinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:01:57Zoai:ri.conicet.gov.ar:11336/154163instacron: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 10:01:57.865CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
title Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
spellingShingle Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
Cardenas, Sofía
CANCER DE PROSTATA
EICOSANOIDES
SEÑALES INTRACELULARES
RECEPTOR GPR75
title_short Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
title_full Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
title_fullStr Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
title_full_unstemmed Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
title_sort Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells
dc.creator.none.fl_str_mv Cardenas, Sofía
Colombero, Cecilia
Panelo, Laura Carolina
Dakarapu, Rambabu
Falck, John
Costas, Monica Alejandra
Nowicki, Susana
author Cardenas, Sofía
author_facet Cardenas, Sofía
Colombero, Cecilia
Panelo, Laura Carolina
Dakarapu, Rambabu
Falck, John
Costas, Monica Alejandra
Nowicki, Susana
author_role author
author2 Colombero, Cecilia
Panelo, Laura Carolina
Dakarapu, Rambabu
Falck, John
Costas, Monica Alejandra
Nowicki, Susana
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv CANCER DE PROSTATA
EICOSANOIDES
SEÑALES INTRACELULARES
RECEPTOR GPR75
topic CANCER DE PROSTATA
EICOSANOIDES
SEÑALES INTRACELULARES
RECEPTOR GPR75
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 20-HETE, the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to identify intracellular signaling molecules activated upon GPR75 stimulation by 20-HETE in PC-3 cells.Cells were incubated with 20-HETE (0.1 nM) in the presence or absence of the antagonist of the 20-HETE receptor, AAA (5 or 10 uM). Protein expression of the inducible focal adhesion protein Hydrogen Peroxide Inducible Clone-5 (HIC-5), the phosphorylated and total form of NF-kB, AKT, p38 MAP-Kinase (p38) and EGFR were assessed by western blot. Intracellular localization of p-AKT, NF-kB and PKCa were determined by immunofluorescence and subcellular fractionation. Migration of PC-3 cells incubated with diferentes inhibitors were evaluated by scratch wound healing assay. Results were analyzed using one-way ANOVA followed by Dunnet?s.Incubation with 20-HETE (2 h) increased the phosphorylation of EGFR, NF-kB and AKT by 146, 172 and 219%, respectively (vs control, p<0.01 for NF-kB, and p<0.001 for EGFR and AKT, n=3), and this was inhibited by AAA (vs 20-HETE alone, p<0.05 for NF-kB, p<0.01 for AKT and p<0.001 for EGFR). AAA alone increased p-38 phosphorylation by 248% (p<0.001 vs control, n=3). 20-HETE (1 h) induced the translocation of p-AKT to the nuclei (p<0.001, n=3) and promoted the redistribution of PKCa out of the nuclei (p<0.05, n=3) to the plasma membrane (p<0.001). Both effects were inhibited by AAA (vs 20-HETE, p<0.01 for AKT and p<0.05 for PKCa). AAA alone reduced the nuclear signal of p-AKT and NF-kB usually activated in tumoral cells (p<0.001 for both, n=3). Additionally, 20-HETE (12 h) increased by 150% the protein expression of Hic-5 (p<0.0001, n=5) and this was abolished by AAA (p<0.001).Our results show that 20-HETE modulates signaling pathways known to be deregulated in malignant cells through the GPR75-axis.
Fil: Cardenas, Sofía. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Fil: Colombero, Cecilia. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Fil: Panelo, Laura Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Dakarapu, Rambabu. University of Texas. Southwestern Medical Center; Estados Unidos
Fil: Falck, John. University of Texas. Southwestern Medical Center; Estados Unidos
Fil: Costas, Monica Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Médicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Médicas; Argentina
Fil: Nowicki, Susana. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Gobierno de la Ciudad de Buenos Aires. Centro de Investigaciones Endocrinológicas "Dr. César Bergada". Fundación de Endocrinología Infantil. Centro de Investigaciones Endocrinológicas "Dr. César Bergada"; Argentina
Reunión anual de las Sociedades de Biociencia
Mar del Plata
Argentina
Sociedad Argentina de Investigación Clínica
Asociación Argentina de Farmacología Experimental
Sociedad Argentina de Biología
Asociación Argentina de Ciencia y Tecnología de Animales de Laboratorio
Sociedad Argentina de Protozoología
description 20-HETE, the product of 20-hydroxylation of arachidonic acid by cytochrome P450 isoforms (CYP4F2 and CYP4A11), has a role in the oncogenesis of several human tumors. Recently, the GPR75 receptor has been identified as the target for 20-HETE. We have shown that androgen independent prostate cancer cells (PC-3) express GPR75. The aim of this study was to identify intracellular signaling molecules activated upon GPR75 stimulation by 20-HETE in PC-3 cells.Cells were incubated with 20-HETE (0.1 nM) in the presence or absence of the antagonist of the 20-HETE receptor, AAA (5 or 10 uM). Protein expression of the inducible focal adhesion protein Hydrogen Peroxide Inducible Clone-5 (HIC-5), the phosphorylated and total form of NF-kB, AKT, p38 MAP-Kinase (p38) and EGFR were assessed by western blot. Intracellular localization of p-AKT, NF-kB and PKCa were determined by immunofluorescence and subcellular fractionation. Migration of PC-3 cells incubated with diferentes inhibitors were evaluated by scratch wound healing assay. Results were analyzed using one-way ANOVA followed by Dunnet?s.Incubation with 20-HETE (2 h) increased the phosphorylation of EGFR, NF-kB and AKT by 146, 172 and 219%, respectively (vs control, p<0.01 for NF-kB, and p<0.001 for EGFR and AKT, n=3), and this was inhibited by AAA (vs 20-HETE alone, p<0.05 for NF-kB, p<0.01 for AKT and p<0.001 for EGFR). AAA alone increased p-38 phosphorylation by 248% (p<0.001 vs control, n=3). 20-HETE (1 h) induced the translocation of p-AKT to the nuclei (p<0.001, n=3) and promoted the redistribution of PKCa out of the nuclei (p<0.05, n=3) to the plasma membrane (p<0.001). Both effects were inhibited by AAA (vs 20-HETE, p<0.01 for AKT and p<0.05 for PKCa). AAA alone reduced the nuclear signal of p-AKT and NF-kB usually activated in tumoral cells (p<0.001 for both, n=3). Additionally, 20-HETE (12 h) increased by 150% the protein expression of Hic-5 (p<0.0001, n=5) and this was abolished by AAA (p<0.001).Our results show that 20-HETE modulates signaling pathways known to be deregulated in malignant cells through the GPR75-axis.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/publishedVersion
info:eu-repo/semantics/conferenceObject
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http://purl.org/coar/resource_type/c_5794
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status_str publishedVersion
format conferenceObject
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/154163
Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells; Reunión anual de las Sociedades de Biociencia; Mar del Plata; Argentina; 2019; 82-82
0025-7680
1669-9106
CONICET Digital
CONICET
url http://hdl.handle.net/11336/154163
identifier_str_mv Intracellular signaling pathways triggered by the stimulation of the G-coupled Protein Receptor GPR75 by 20-hydroxyeicosatetraenoic acid (20-HETE) in androgen independent prostate cancer cells; Reunión anual de las Sociedades de Biociencia; Mar del Plata; Argentina; 2019; 82-82
0025-7680
1669-9106
CONICET Digital
CONICET
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language spa
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dc.publisher.none.fl_str_mv Fundación Revista Medicina
publisher.none.fl_str_mv Fundación Revista Medicina
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