Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilid...
- Autores
- Díaz Bessone, María Inés
- Año de publicación
- 2016
- Idioma
- español castellano
- Tipo de recurso
- tesis doctoral
- Estado
- versión publicada
- Colaborador/a o director/a de tesis
- Urtreger, Alejandro Jorge
Todaro, Laura Beatriz - Descripción
- Breast cancer represents the most common kind of cancer in women and it is estimatedthat more than one million new cases are diagnosed each year worldwide. It is a complexdisease, which presents a variety of subgroups with different genetic and histopathologicfeatures and therefore with different responses to treatments. Multiple signaling pathways are involved in malignant progression. Some of them arepromising targets for therapeutic intervention, including protein kinase C (PKC), involvedin cellular events such as proliferation, differentiation and apoptosis and the retinoidsystem, widely implicated in cell differentiation. Since different mammary malignancies exhibit differential expression of PKC isoforms, wehave developed (human and murine) mammary cell models overexpressing α or δ PKCisoforms. Using these models we studied how PKCα or PKCδ alters cell parametersassociated with tumor progression and metastatic dissemination while we assessed theresponse to treatment with retinoids (ATRA). Our results suggest that PKCα overexpression confers to the cells a retinoic acid-sensitivephenotype, through an arrest in the G0 / G1 phase of the cell cycle. Overexpression of PKCδ, in MDA-MB231 cells, induced a less aggressive phenotype, significantly reducing itsinvasive capability. Finally the lack of response of this cell line to ATRA treatment could bedue to the inability to trans-repress AP-1 sites.
Fil: Díaz Bessone, María Inés. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. - Materia
-
CANCER DE MAMA
PROTEINA QUINASA C
ACIDO RETINOICO
BREAST CANCER
PROTEIN KINASE C
RETINOIC ACID - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar
- Repositorio
- Institución
- Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
- OAI Identificador
- tesis:tesis_n6034_DiazBessone
Ver los metadatos del registro completo
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spelling |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoidesEffect of overexpression of different isoforms of Protein Kinase C (PKC) in modulation of malignant phenotype of mammary ephitelial cells. Alteration in sensitivity to treatment with retinoidsDíaz Bessone, María InésCANCER DE MAMAPROTEINA QUINASA CACIDO RETINOICOBREAST CANCERPROTEIN KINASE CRETINOIC ACIDBreast cancer represents the most common kind of cancer in women and it is estimatedthat more than one million new cases are diagnosed each year worldwide. It is a complexdisease, which presents a variety of subgroups with different genetic and histopathologicfeatures and therefore with different responses to treatments. Multiple signaling pathways are involved in malignant progression. Some of them arepromising targets for therapeutic intervention, including protein kinase C (PKC), involvedin cellular events such as proliferation, differentiation and apoptosis and the retinoidsystem, widely implicated in cell differentiation. Since different mammary malignancies exhibit differential expression of PKC isoforms, wehave developed (human and murine) mammary cell models overexpressing α or δ PKCisoforms. Using these models we studied how PKCα or PKCδ alters cell parametersassociated with tumor progression and metastatic dissemination while we assessed theresponse to treatment with retinoids (ATRA). Our results suggest that PKCα overexpression confers to the cells a retinoic acid-sensitivephenotype, through an arrest in the G0 / G1 phase of the cell cycle. Overexpression of PKCδ, in MDA-MB231 cells, induced a less aggressive phenotype, significantly reducing itsinvasive capability. Finally the lack of response of this cell line to ATRA treatment could bedue to the inability to trans-repress AP-1 sites.Fil: Díaz Bessone, María Inés. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina.Universidad de Buenos Aires. Facultad de Ciencias Exactas y NaturalesUrtreger, Alejandro JorgeTodaro, Laura Beatriz2016-03-28info:eu-repo/semantics/doctoralThesisinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_db06info:ar-repo/semantics/tesisDoctoralapplication/pdfhttps://hdl.handle.net/20.500.12110/tesis_n6034_DiazBessonespainfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/arreponame:Biblioteca Digital (UBA-FCEN)instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesinstacron:UBA-FCEN2025-09-29T13:42:14Ztesis:tesis_n6034_DiazBessoneInstitucionalhttps://digital.bl.fcen.uba.ar/Universidad públicaNo correspondehttps://digital.bl.fcen.uba.ar/cgi-bin/oaiserver.cgiana@bl.fcen.uba.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:18962025-09-29 13:42:15.771Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturalesfalse |
dc.title.none.fl_str_mv |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides Effect of overexpression of different isoforms of Protein Kinase C (PKC) in modulation of malignant phenotype of mammary ephitelial cells. Alteration in sensitivity to treatment with retinoids |
title |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
spellingShingle |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides Díaz Bessone, María Inés CANCER DE MAMA PROTEINA QUINASA C ACIDO RETINOICO BREAST CANCER PROTEIN KINASE C RETINOIC ACID |
title_short |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
title_full |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
title_fullStr |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
title_full_unstemmed |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
title_sort |
Efecto de la sobreexpresión de distintas isoformas de la Proteína Quinasa C (PKC) en la modulación del fenotipo maligno de células mamarias epiteliales. Alteración en la sensibilidad al tratamiento con retinoides |
dc.creator.none.fl_str_mv |
Díaz Bessone, María Inés |
author |
Díaz Bessone, María Inés |
author_facet |
Díaz Bessone, María Inés |
author_role |
author |
dc.contributor.none.fl_str_mv |
Urtreger, Alejandro Jorge Todaro, Laura Beatriz |
dc.subject.none.fl_str_mv |
CANCER DE MAMA PROTEINA QUINASA C ACIDO RETINOICO BREAST CANCER PROTEIN KINASE C RETINOIC ACID |
topic |
CANCER DE MAMA PROTEINA QUINASA C ACIDO RETINOICO BREAST CANCER PROTEIN KINASE C RETINOIC ACID |
dc.description.none.fl_txt_mv |
Breast cancer represents the most common kind of cancer in women and it is estimatedthat more than one million new cases are diagnosed each year worldwide. It is a complexdisease, which presents a variety of subgroups with different genetic and histopathologicfeatures and therefore with different responses to treatments. Multiple signaling pathways are involved in malignant progression. Some of them arepromising targets for therapeutic intervention, including protein kinase C (PKC), involvedin cellular events such as proliferation, differentiation and apoptosis and the retinoidsystem, widely implicated in cell differentiation. Since different mammary malignancies exhibit differential expression of PKC isoforms, wehave developed (human and murine) mammary cell models overexpressing α or δ PKCisoforms. Using these models we studied how PKCα or PKCδ alters cell parametersassociated with tumor progression and metastatic dissemination while we assessed theresponse to treatment with retinoids (ATRA). Our results suggest that PKCα overexpression confers to the cells a retinoic acid-sensitivephenotype, through an arrest in the G0 / G1 phase of the cell cycle. Overexpression of PKCδ, in MDA-MB231 cells, induced a less aggressive phenotype, significantly reducing itsinvasive capability. Finally the lack of response of this cell line to ATRA treatment could bedue to the inability to trans-repress AP-1 sites. Fil: Díaz Bessone, María Inés. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. |
description |
Breast cancer represents the most common kind of cancer in women and it is estimatedthat more than one million new cases are diagnosed each year worldwide. It is a complexdisease, which presents a variety of subgroups with different genetic and histopathologicfeatures and therefore with different responses to treatments. Multiple signaling pathways are involved in malignant progression. Some of them arepromising targets for therapeutic intervention, including protein kinase C (PKC), involvedin cellular events such as proliferation, differentiation and apoptosis and the retinoidsystem, widely implicated in cell differentiation. Since different mammary malignancies exhibit differential expression of PKC isoforms, wehave developed (human and murine) mammary cell models overexpressing α or δ PKCisoforms. Using these models we studied how PKCα or PKCδ alters cell parametersassociated with tumor progression and metastatic dissemination while we assessed theresponse to treatment with retinoids (ATRA). Our results suggest that PKCα overexpression confers to the cells a retinoic acid-sensitivephenotype, through an arrest in the G0 / G1 phase of the cell cycle. Overexpression of PKCδ, in MDA-MB231 cells, induced a less aggressive phenotype, significantly reducing itsinvasive capability. Finally the lack of response of this cell line to ATRA treatment could bedue to the inability to trans-repress AP-1 sites. |
publishDate |
2016 |
dc.date.none.fl_str_mv |
2016-03-28 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/doctoralThesis info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_db06 info:ar-repo/semantics/tesisDoctoral |
format |
doctoralThesis |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
https://hdl.handle.net/20.500.12110/tesis_n6034_DiazBessone |
url |
https://hdl.handle.net/20.500.12110/tesis_n6034_DiazBessone |
dc.language.none.fl_str_mv |
spa |
language |
spa |
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 |
dc.publisher.none.fl_str_mv |
Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
publisher.none.fl_str_mv |
Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
dc.source.none.fl_str_mv |
reponame:Biblioteca Digital (UBA-FCEN) instname:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales instacron:UBA-FCEN |
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Biblioteca Digital (UBA-FCEN) |
collection |
Biblioteca Digital (UBA-FCEN) |
instname_str |
Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
instacron_str |
UBA-FCEN |
institution |
UBA-FCEN |
repository.name.fl_str_mv |
Biblioteca Digital (UBA-FCEN) - Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales |
repository.mail.fl_str_mv |
ana@bl.fcen.uba.ar |
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