Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidoni...

Autores: Comba, Andrea; Almada, Luciana Victoria; Tolosa, Ezequiel J.; Iguchi, Eriko; Marks, David L.; Vara Messler, Marianela; Silva, Renata Alejandra; Fernandez-Barrena, Maite G.; Enriquez-Hesles, Elisa; Vrabel, Anne L.; Botta, Bruno; Di Marcotulio, Lucia; Ellenrieder, Volker; Eynard, Aldo Renato; Pasqualini, María Eugenia; Fernandez Zapico, Martin Ernesto
Año de publicación: 2016
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1BB, in AA-treated cells.Wedemonstrated that down-regulation of the transcription factor gliomaassociated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability, and expression of antiapoptotic molecules. Further characterization showed thatAArepresses GLI1 expression by stimulating nuclear translocation of NFATc1, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants impaired the AAinduced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for future PUFA-based therapeutic approaches.
Fil: Comba, Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Almada, Luciana Victoria. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Tolosa, Ezequiel J.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Iguchi, Eriko. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Marks, David L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Vara Messler, Marianela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Silva, Renata Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Fernandez-Barrena, Maite G.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Enriquez-Hesles, Elisa. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Vrabel, Anne L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Fil: Botta, Bruno. Sapienza University; Italia
Fil: Di Marcotulio, Lucia. Sapienza University; Italia
Fil: Ellenrieder, Volker. University Medical Center Göttingen; Alemania
Fil: Eynard, Aldo Renato. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Pasqualini, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina
Fil: Fernandez Zapico, Martin Ernesto. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
Materia: GLI1
ARACHIDONIC ACID
CANCER
APOPTOSIS
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/130675

Acceder

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repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acidComba, AndreaAlmada, Luciana VictoriaTolosa, Ezequiel J.Iguchi, ErikoMarks, David L.Vara Messler, MarianelaSilva, Renata AlejandraFernandez-Barrena, Maite G.Enriquez-Hesles, ElisaVrabel, Anne L.Botta, BrunoDi Marcotulio, LuciaEllenrieder, VolkerEynard, Aldo RenatoPasqualini, María EugeniaFernandez Zapico, Martin ErnestoGLI1ARACHIDONIC ACIDCANCERAPOPTOSIShttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1BB, in AA-treated cells.Wedemonstrated that down-regulation of the transcription factor gliomaassociated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability, and expression of antiapoptotic molecules. Further characterization showed thatAArepresses GLI1 expression by stimulating nuclear translocation of NFATc1, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants impaired the AAinduced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for future PUFA-based therapeutic approaches.Fil: Comba, Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Almada, Luciana Victoria. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Tolosa, Ezequiel J.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Iguchi, Eriko. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Marks, David L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Vara Messler, Marianela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Silva, Renata Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Fernandez-Barrena, Maite G.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Enriquez-Hesles, Elisa. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Vrabel, Anne L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosFil: Botta, Bruno. Sapienza University; ItaliaFil: Di Marcotulio, Lucia. Sapienza University; ItaliaFil: Ellenrieder, Volker. University Medical Center Göttingen; AlemaniaFil: Eynard, Aldo Renato. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Pasqualini, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; ArgentinaFil: Fernandez Zapico, Martin Ernesto. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados UnidosAmerican Society for Biochemistry and Molecular Biology2016-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/130675Comba, Andrea; Almada, Luciana Victoria; Tolosa, Ezequiel J.; Iguchi, Eriko; Marks, David L.; et al.; Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid; American Society for Biochemistry and Molecular Biology; Journal of Biological Chemistry (online); 291; 4; 1-2016; 1933-19470021-92581083-351XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.jbc.org/content/early/2015/11/24/jbc.M115.691972.longinfo:eu-repo/semantics/altIdentifier/doi/10.1074/jbc.M115.691972info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T11:46:56Zoai:ri.conicet.gov.ar:11336/130675instacron: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:34982025-10-22 11:46:56.955CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
title	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
spellingShingle	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid Comba, Andrea GLI1 ARACHIDONIC ACID CANCER APOPTOSIS
title_short	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
title_full	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
title_fullStr	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
title_full_unstemmed	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
title_sort	Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid
dc.creator.none.fl_str_mv	Comba, Andrea Almada, Luciana Victoria Tolosa, Ezequiel J. Iguchi, Eriko Marks, David L. Vara Messler, Marianela Silva, Renata Alejandra Fernandez-Barrena, Maite G. Enriquez-Hesles, Elisa Vrabel, Anne L. Botta, Bruno Di Marcotulio, Lucia Ellenrieder, Volker Eynard, Aldo Renato Pasqualini, María Eugenia Fernandez Zapico, Martin Ernesto
author	Comba, Andrea
author_facet	Comba, Andrea Almada, Luciana Victoria Tolosa, Ezequiel J. Iguchi, Eriko Marks, David L. Vara Messler, Marianela Silva, Renata Alejandra Fernandez-Barrena, Maite G. Enriquez-Hesles, Elisa Vrabel, Anne L. Botta, Bruno Di Marcotulio, Lucia Ellenrieder, Volker Eynard, Aldo Renato Pasqualini, María Eugenia Fernandez Zapico, Martin Ernesto
author_role	author
author2	Almada, Luciana Victoria Tolosa, Ezequiel J. Iguchi, Eriko Marks, David L. Vara Messler, Marianela Silva, Renata Alejandra Fernandez-Barrena, Maite G. Enriquez-Hesles, Elisa Vrabel, Anne L. Botta, Bruno Di Marcotulio, Lucia Ellenrieder, Volker Eynard, Aldo Renato Pasqualini, María Eugenia Fernandez Zapico, Martin Ernesto
author2_role	author author author author author author author author author author author author author author author
dc.subject.none.fl_str_mv	GLI1 ARACHIDONIC ACID CANCER APOPTOSIS
topic	GLI1 ARACHIDONIC ACID CANCER APOPTOSIS
purl_subject.fl_str_mv	https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv	Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1BB, in AA-treated cells.Wedemonstrated that down-regulation of the transcription factor gliomaassociated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability, and expression of antiapoptotic molecules. Further characterization showed thatAArepresses GLI1 expression by stimulating nuclear translocation of NFATc1, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants impaired the AAinduced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for future PUFA-based therapeutic approaches. Fil: Comba, Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina Fil: Almada, Luciana Victoria. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Tolosa, Ezequiel J.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Iguchi, Eriko. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Marks, David L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Vara Messler, Marianela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina Fil: Silva, Renata Alejandra. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina Fil: Fernandez-Barrena, Maite G.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Enriquez-Hesles, Elisa. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Vrabel, Anne L.. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos Fil: Botta, Bruno. Sapienza University; Italia Fil: Di Marcotulio, Lucia. Sapienza University; Italia Fil: Ellenrieder, Volker. University Medical Center Göttingen; Alemania Fil: Eynard, Aldo Renato. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina Fil: Pasqualini, María Eugenia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina Fil: Fernandez Zapico, Martin Ernesto. Mayo Clinic - Schuze Center Of Novel Therapeutic; Estados Unidos
description	Numerous reports have demonstrated a tumor inhibitory effect of polyunsaturated fatty acids (PUFAs). However, the molecular mechanisms modulating this phenomenon are in part poorly understood. Here, we provide evidence of a novel antitumoral mechanism of the PUFA arachidonic acid (AA). In vivo and in vitro experiments showed that AA treatment decreased tumor growth and metastasis and increased apoptosis. Molecular analysis of this effect showed significantly reduced expression of a subset of antiapoptotic proteins, including BCL2, BFL1/A1, and 4-1BB, in AA-treated cells.Wedemonstrated that down-regulation of the transcription factor gliomaassociated protein 1 (GLI1) in AA-treated cells is the underlying mechanism controlling BCL2, BFL1/A1, and 4-1BB expression. Using luciferase reporters, chromatin immunoprecipitation, and expression studies, we found that GLI1 binds to the promoter of these antiapoptotic molecules and regulates their expression and promoter activity. We provide evidence that AA-induced apoptosis and down-regulation of antiapoptotic genes can be inhibited by overexpressing GLI1 in AA-sensitive cells. Conversely, inhibition of GLI1 mimics AA treatments, leading to decreased tumor growth, cell viability, and expression of antiapoptotic molecules. Further characterization showed thatAArepresses GLI1 expression by stimulating nuclear translocation of NFATc1, which then binds the GLI1 promoter and represses its transcription. AA was shown to increase reactive oxygen species. Treatment with antioxidants impaired the AAinduced apoptosis and down-regulation of GLI1 and NFATc1 activation, indicating that NFATc1 activation and GLI1 repression require the generation of reactive oxygen species. Collectively, these results define a novel mechanism underlying AA antitumoral functions that may serve as a foundation for future PUFA-based therapeutic approaches.
publishDate	2016
dc.date.none.fl_str_mv	2016-01
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/11336/130675 Comba, Andrea; Almada, Luciana Victoria; Tolosa, Ezequiel J.; Iguchi, Eriko; Marks, David L.; et al.; Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid; American Society for Biochemistry and Molecular Biology; Journal of Biological Chemistry (online); 291; 4; 1-2016; 1933-1947 0021-9258 1083-351X CONICET Digital CONICET
url	http://hdl.handle.net/11336/130675
identifier_str_mv	Comba, Andrea; Almada, Luciana Victoria; Tolosa, Ezequiel J.; Iguchi, Eriko; Marks, David L.; et al.; Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidonic acid; American Society for Biochemistry and Molecular Biology; Journal of Biological Chemistry (online); 291; 4; 1-2016; 1933-1947 0021-9258 1083-351X CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/url/http://www.jbc.org/content/early/2015/11/24/jbc.M115.691972.long info:eu-repo/semantics/altIdentifier/doi/10.1074/jbc.M115.691972
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 application/pdf application/pdf application/pdf
dc.publisher.none.fl_str_mv	American Society for Biochemistry and Molecular Biology
publisher.none.fl_str_mv	American Society for Biochemistry and Molecular Biology
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
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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
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Nuclear factor of activated T cells-dependent downregulation of the transcription factor glioma-associated protein 1 (GLI1) underlies the growth inhibitory properties of arachidoni...

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