Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression

Autores
Pino, María T. L.; Verstraeten, Sandra Viviana
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The effects of thallium [Tl(I) and Tl(III)] on the PC12 cell cycle were evaluated without (EGF−) or with (EGF+) media supplementation with epidermal growth factor (EGF). The following markers of cell-cycle phases were analyzed: cyclin D1 (G1); E2F-1, cyclin E and cytosolic p21 (G1→S transition); nuclear PCNA and cyclin A (S); and cyclin B1 (G2). The amount of cells in each phase and the activation of the signaling cascade triggered by EGF were also analyzed. Tl(I) and Tl(III) (5–100 μM) caused dissimilar effects on PC12 cell proliferation. In EGF− cells, Tl(I) increased the expression of G1→S transition markers and nuclear PCNA, without affecting cyclin A or cyclin B1. In addition to those, cyclin B1 was also increased in EGF+ cells. In EGF− cells, Tl(III) increased the expression of cyclin D1, all the G1→S and S phase markers and cyclin B1. In EGF+ cells, Tl(III) increased cyclin D1 expression and decreased all the markers of G1→S transition and the S phase. Even when these cations did not induce the activation of EGF receptor (EGFR) in EGF− cells, they promoted the phosphorylation of ERK1/2 and Akt. In the presence of EGF, the cations anticipated EGFR phosphorylation without affecting the kinetics of EGF-dependent ERK1/2 and Akt phosphorylation. Altogether, results indicate that Tl(I) promoted cell proliferation in both EGF− and EGF+ cells. In contrast, Tl(III) promoted the proliferation of EGF− cells but delayed it in EGF+ cells, which may be related to the toxic effects of this cation in PC12 cells.
Fil: Pino, María T. L.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina
Fil: Verstraeten, Sandra Viviana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
Materia
Cell Cycle
Cell Signaling
Cyclins
Epidermal Growth Factor
Thallium
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:11336/18263
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/18263
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progressionPino, María T. L.Verstraeten, Sandra VivianaCell CycleCell SignalingCyclinsEpidermal Growth FactorThalliumhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1The effects of thallium [Tl(I) and Tl(III)] on the PC12 cell cycle were evaluated without (EGF−) or with (EGF+) media supplementation with epidermal growth factor (EGF). The following markers of cell-cycle phases were analyzed: cyclin D1 (G1); E2F-1, cyclin E and cytosolic p21 (G1→S transition); nuclear PCNA and cyclin A (S); and cyclin B1 (G2). The amount of cells in each phase and the activation of the signaling cascade triggered by EGF were also analyzed. Tl(I) and Tl(III) (5–100 μM) caused dissimilar effects on PC12 cell proliferation. In EGF− cells, Tl(I) increased the expression of G1→S transition markers and nuclear PCNA, without affecting cyclin A or cyclin B1. In addition to those, cyclin B1 was also increased in EGF+ cells. In EGF− cells, Tl(III) increased the expression of cyclin D1, all the G1→S and S phase markers and cyclin B1. In EGF+ cells, Tl(III) increased cyclin D1 expression and decreased all the markers of G1→S transition and the S phase. Even when these cations did not induce the activation of EGF receptor (EGFR) in EGF− cells, they promoted the phosphorylation of ERK1/2 and Akt. In the presence of EGF, the cations anticipated EGFR phosphorylation without affecting the kinetics of EGF-dependent ERK1/2 and Akt phosphorylation. Altogether, results indicate that Tl(I) promoted cell proliferation in both EGF− and EGF+ cells. In contrast, Tl(III) promoted the proliferation of EGF− cells but delayed it in EGF+ cells, which may be related to the toxic effects of this cation in PC12 cells.Fil: Pino, María T. L.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; ArgentinaFil: Verstraeten, Sandra Viviana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaWiley2015-08info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/18263Pino, María T. L.; Verstraeten, Sandra Viviana; Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression; Wiley; Journal of Applied Toxicology; 35; 8; 8-2015; 952-9690260-437XCONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1002/jat.3096/abstractinfo:eu-repo/semantics/altIdentifier/doi/10.1002/jat.3096info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:42:02Zoai:ri.conicet.gov.ar:11336/18263instacron: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:34982025-09-29 10:42:02.552CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
title Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
spellingShingle Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
Pino, María T. L.
Cell Cycle
Cell Signaling
Cyclins
Epidermal Growth Factor
Thallium
title_short Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
title_full Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
title_fullStr Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
title_full_unstemmed Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
title_sort Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression
dc.creator.none.fl_str_mv Pino, María T. L.
Verstraeten, Sandra Viviana
author Pino, María T. L.
author_facet Pino, María T. L.
Verstraeten, Sandra Viviana
author_role author
author2 Verstraeten, Sandra Viviana
author2_role author
dc.subject.none.fl_str_mv Cell Cycle
Cell Signaling
Cyclins
Epidermal Growth Factor
Thallium
topic Cell Cycle
Cell Signaling
Cyclins
Epidermal Growth Factor
Thallium
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 effects of thallium [Tl(I) and Tl(III)] on the PC12 cell cycle were evaluated without (EGF−) or with (EGF+) media supplementation with epidermal growth factor (EGF). The following markers of cell-cycle phases were analyzed: cyclin D1 (G1); E2F-1, cyclin E and cytosolic p21 (G1→S transition); nuclear PCNA and cyclin A (S); and cyclin B1 (G2). The amount of cells in each phase and the activation of the signaling cascade triggered by EGF were also analyzed. Tl(I) and Tl(III) (5–100 μM) caused dissimilar effects on PC12 cell proliferation. In EGF− cells, Tl(I) increased the expression of G1→S transition markers and nuclear PCNA, without affecting cyclin A or cyclin B1. In addition to those, cyclin B1 was also increased in EGF+ cells. In EGF− cells, Tl(III) increased the expression of cyclin D1, all the G1→S and S phase markers and cyclin B1. In EGF+ cells, Tl(III) increased cyclin D1 expression and decreased all the markers of G1→S transition and the S phase. Even when these cations did not induce the activation of EGF receptor (EGFR) in EGF− cells, they promoted the phosphorylation of ERK1/2 and Akt. In the presence of EGF, the cations anticipated EGFR phosphorylation without affecting the kinetics of EGF-dependent ERK1/2 and Akt phosphorylation. Altogether, results indicate that Tl(I) promoted cell proliferation in both EGF− and EGF+ cells. In contrast, Tl(III) promoted the proliferation of EGF− cells but delayed it in EGF+ cells, which may be related to the toxic effects of this cation in PC12 cells.
Fil: Pino, María T. L.. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina
Fil: Verstraeten, Sandra Viviana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Química Biológica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; Argentina
description The effects of thallium [Tl(I) and Tl(III)] on the PC12 cell cycle were evaluated without (EGF−) or with (EGF+) media supplementation with epidermal growth factor (EGF). The following markers of cell-cycle phases were analyzed: cyclin D1 (G1); E2F-1, cyclin E and cytosolic p21 (G1→S transition); nuclear PCNA and cyclin A (S); and cyclin B1 (G2). The amount of cells in each phase and the activation of the signaling cascade triggered by EGF were also analyzed. Tl(I) and Tl(III) (5–100 μM) caused dissimilar effects on PC12 cell proliferation. In EGF− cells, Tl(I) increased the expression of G1→S transition markers and nuclear PCNA, without affecting cyclin A or cyclin B1. In addition to those, cyclin B1 was also increased in EGF+ cells. In EGF− cells, Tl(III) increased the expression of cyclin D1, all the G1→S and S phase markers and cyclin B1. In EGF+ cells, Tl(III) increased cyclin D1 expression and decreased all the markers of G1→S transition and the S phase. Even when these cations did not induce the activation of EGF receptor (EGFR) in EGF− cells, they promoted the phosphorylation of ERK1/2 and Akt. In the presence of EGF, the cations anticipated EGFR phosphorylation without affecting the kinetics of EGF-dependent ERK1/2 and Akt phosphorylation. Altogether, results indicate that Tl(I) promoted cell proliferation in both EGF− and EGF+ cells. In contrast, Tl(III) promoted the proliferation of EGF− cells but delayed it in EGF+ cells, which may be related to the toxic effects of this cation in PC12 cells.
publishDate 2015
dc.date.none.fl_str_mv 2015-08
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/11336/18263
Pino, María T. L.; Verstraeten, Sandra Viviana; Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression; Wiley; Journal of Applied Toxicology; 35; 8; 8-2015; 952-969
0260-437X
CONICET Digital
CONICET
url http://hdl.handle.net/11336/18263
identifier_str_mv Pino, María T. L.; Verstraeten, Sandra Viviana; Tl(I) and Tl(III) alter the expression of EGF-dependent signals and cyclins required for pheochromocytoma (PC12) cell-cycle resumption and progression; Wiley; Journal of Applied Toxicology; 35; 8; 8-2015; 952-969
0260-437X
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://onlinelibrary.wiley.com/doi/10.1002/jat.3096/abstract
info:eu-repo/semantics/altIdentifier/doi/10.1002/jat.3096
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
dc.publisher.none.fl_str_mv Wiley
publisher.none.fl_str_mv Wiley
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
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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score 13.070432

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