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Artículo

Involvement of MEK/ERK1/2 and PI3K/Akt pathways in the refractory behavior of GH3B6 Pituitary tumor cells to the inhibitory effect of TGFß1

Petiti, Juan PabloIcon ; del Valle Sosa, Liliana; Sabatino, María EugeniaIcon ; Vaca, Alicia Maldré del ValleIcon ; Gutiérrez, SilvinaIcon ; de Paul, Ana LuciaIcon ; Torres, Alicia InesIcon
Fecha de publicación: 02/2015
Editorial: Endocrine Society
Revista: Endocrinology
ISSN: 0013-7227
e-ISSN: 1945-7170
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Bioquímica y Biología Molecular

Resumen

Pituitary tumor cells have a poor response to the growth inhibitory effect of TGFβ1, possibly resulting from the cross talk of TGFβ/Smads signal with other signaling pathways, an undescribed mechanism in these tumoral cells. To address this hypothesis, we investigated whether the mitogen-activated extracellular signal-regulated kinase (MEK)/ERK1/2 and phosphoinositide-3 kinase/protein kinase B (PI3K/Akt) pathways were able to regulate the antimitogenic effect of TGFβ1 on GH3B6 cells. TGFβ1 treatment decreased the cell proliferation and induced an activation of mothers against decapentaplegic homolog 2/3 (Smad2/3), effects that were potentiated by MEK and PI3K inhibitors, thus indicating the existence of a cross talk between TGFβ1/Smad with the MEK/ERK1/2 or PI3K/Akt pathways. In addition, through immunoprecipitation assays, a direct interaction was observed between Smad2/3-ERK1/2 and Smad2/3-Akt, which decreased when the GH3B6 cells were incubated with TGFβ1 in the presence of MEK or PI3K inhibitors, thereby suggesting that the ERK1/2- and Akt-activated states were involved. These Smad2/3-ERK1/2 and Smad2/3-Akt associations were also confirmed by confocal and transmission electron microscopy. These findings indicate that the TGFβ1-antimitogenic effect in GH3B6 cells was attenuated by the MEK/ERK1/2 and PI3K/Akt pathways via modulating Smad2/3 phosphorylation. This molecular mechanism could explain in part the refractory behavior of pituitary tumor cells to the inhibitory effect of TGFβ1.
Palabras clave: Tgfβ1 , Smad2/3 , Proliferation , Transmission Electron Microscopy , Pituitary Tumor
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/11598
DOI: http://dx.doi.org/10.1210/en.2014-1070
URL: http://press.endocrine.org/doi/abs/10.1210/en.2014-1070
Colecciones
Articulos(INICSA)
Articulos de INSTITUTO DE INVESTIGACIONES EN CIENCIAS DE LA SALUD
Citación
Petiti, Juan Pablo; del Valle Sosa, Liliana; Sabatino, María Eugenia; Vaca, Alicia Maldré del Valle; Gutiérrez, Silvina; et al.; Involvement of MEK/ERK1/2 and PI3K/Akt pathways in the refractory behavior of GH3B6 Pituitary tumor cells to the inhibitory effect of TGFß1; Endocrine Society; Endocrinology; 156; 2; 2-2015; 534-547
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