Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation

Autores
Dekanty, Andres; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, Federico; Barrio, Marcela; Casala, Jorgelina; Paciencia, Mercedes; Rogers, Florencia; Coso, Omar Adrian; Piwien Pilipuk, Graciela; Rudlland, Philip S.; Jimenez de Asua, Luis Adan Felipe
Año de publicación
2006
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2alpha (PGF2alpha) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so. However, LIF and PGF2alpha can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2alpha treatment. PGF2alpha induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2alpha increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2alpha mitogenic action. More importantly, the synergistic effect between LIF and PGF2alpha to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2alpha-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division.
Fil: Dekanty, Andres. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Sauane, Moira. Fundación Instituto Leloir; Argentina
Fil: Cárdenas, Belén. Fundación Instituto Leloir; Argentina
Fil: Coluccio Leskow, Federico. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Barrio, Marcela. Fundación Instituto Leloir; Argentina
Fil: Casala, Jorgelina. Fundación Instituto Leloir; Argentina
Fil: Paciencia, Mercedes. Fundación Instituto Leloir; Argentina
Fil: Rogers, Florencia. Fundación Instituto Leloir; Argentina
Fil: Coso, Omar Adrian. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Piwien Pilipuk, Graciela. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Rudlland, Philip S.. University of Liverpool; Reino Unido
Fil: Jimenez de Asua, Luis Adan Felipe. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
Materia
LIF
PGF2alpha
OSM
MAPK
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:11336/18518

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network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activationDekanty, AndresSauane, MoiraCárdenas, BelénColuccio Leskow, FedericoBarrio, MarcelaCasala, JorgelinaPaciencia, MercedesRogers, FlorenciaCoso, Omar AdrianPiwien Pilipuk, GracielaRudlland, Philip S.Jimenez de Asua, Luis Adan FelipeLIFPGF2alphaOSMMAPKhttps://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2alpha (PGF2alpha) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so. However, LIF and PGF2alpha can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2alpha treatment. PGF2alpha induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2alpha increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2alpha mitogenic action. More importantly, the synergistic effect between LIF and PGF2alpha to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2alpha-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division.Fil: Dekanty, Andres. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Sauane, Moira. Fundación Instituto Leloir; ArgentinaFil: Cárdenas, Belén. Fundación Instituto Leloir; ArgentinaFil: Coluccio Leskow, Federico. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Barrio, Marcela. Fundación Instituto Leloir; ArgentinaFil: Casala, Jorgelina. Fundación Instituto Leloir; ArgentinaFil: Paciencia, Mercedes. Fundación Instituto Leloir; ArgentinaFil: Rogers, Florencia. Fundación Instituto Leloir; ArgentinaFil: Coso, Omar Adrian. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Piwien Pilipuk, Graciela. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Rudlland, Philip S.. University of Liverpool; Reino UnidoFil: Jimenez de Asua, Luis Adan Felipe. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; ArgentinaAmerican Society For Biochemistry And Molecular Biology2006-03-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/18518Dekanty, Andres; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, Federico; Barrio, Marcela; et al.; Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation; American Society For Biochemistry And Molecular Biology; Journal Of Biological Chemistry; 28; 10; 10-3-2006; 6136-61430021-9258CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.jbc.org/content/281/10/6136.longinfo:eu-repo/semantics/altIdentifier/doi/10.1074/jbc.M505839200info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:43:19Zoai:ri.conicet.gov.ar:11336/18518instacron: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 09:43:19.884CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
title Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
spellingShingle Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
Dekanty, Andres
LIF
PGF2alpha
OSM
MAPK
title_short Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
title_full Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
title_fullStr Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
title_full_unstemmed Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
title_sort Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation
dc.creator.none.fl_str_mv Dekanty, Andres
Sauane, Moira
Cárdenas, Belén
Coluccio Leskow, Federico
Barrio, Marcela
Casala, Jorgelina
Paciencia, Mercedes
Rogers, Florencia
Coso, Omar Adrian
Piwien Pilipuk, Graciela
Rudlland, Philip S.
Jimenez de Asua, Luis Adan Felipe
author Dekanty, Andres
author_facet Dekanty, Andres
Sauane, Moira
Cárdenas, Belén
Coluccio Leskow, Federico
Barrio, Marcela
Casala, Jorgelina
Paciencia, Mercedes
Rogers, Florencia
Coso, Omar Adrian
Piwien Pilipuk, Graciela
Rudlland, Philip S.
Jimenez de Asua, Luis Adan Felipe
author_role author
author2 Sauane, Moira
Cárdenas, Belén
Coluccio Leskow, Federico
Barrio, Marcela
Casala, Jorgelina
Paciencia, Mercedes
Rogers, Florencia
Coso, Omar Adrian
Piwien Pilipuk, Graciela
Rudlland, Philip S.
Jimenez de Asua, Luis Adan Felipe
author2_role author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv LIF
PGF2alpha
OSM
MAPK
topic LIF
PGF2alpha
OSM
MAPK
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.2
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2alpha (PGF2alpha) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so. However, LIF and PGF2alpha can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2alpha treatment. PGF2alpha induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2alpha increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2alpha mitogenic action. More importantly, the synergistic effect between LIF and PGF2alpha to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2alpha-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division.
Fil: Dekanty, Andres. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Sauane, Moira. Fundación Instituto Leloir; Argentina
Fil: Cárdenas, Belén. Fundación Instituto Leloir; Argentina
Fil: Coluccio Leskow, Federico. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Barrio, Marcela. Fundación Instituto Leloir; Argentina
Fil: Casala, Jorgelina. Fundación Instituto Leloir; Argentina
Fil: Paciencia, Mercedes. Fundación Instituto Leloir; Argentina
Fil: Rogers, Florencia. Fundación Instituto Leloir; Argentina
Fil: Coso, Omar Adrian. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Departamento de Fisiologia, Biologia Molecular y Celular. Laboratorio de Fisiologia y Biologia Molecular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Piwien Pilipuk, Graciela. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Rudlland, Philip S.. University of Liverpool; Reino Unido
Fil: Jimenez de Asua, Luis Adan Felipe. Fundación Instituto Leloir; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina
description Leukemia inhibitory factor (LIF) and oncostatin M (OSM) induce DNA synthesis in Swiss 3T3 cells through common signaling mechanism(s), whereas other related cytokines such as interleukin-6 and ciliary neurotrophic factor do not cause this response. Induction of DNA replication by LIF or prostaglandin F2alpha (PGF2alpha) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF2alpha fails to do so. However, LIF and PGF2alpha can trigger increases in ERK1/2 activity, which are required for their mitogenic responses because U0126, a MEK1/2 inhibitor, prevents both ERK1/2 activation and induction of DNA synthesis by LIF or PGF2alpha treatment. PGF2alpha induces cyclin D expression and full phosphorylation of retinoblastoma protein. In contrast, LIF fails to promote increases in cyclin D mRNA/protein levels; consequently, LIF induces DNA synthesis without promoting full phosphorylation of retinoblastoma protein (Rb). However, both LIF and PGF2alpha increase cyclin E expression. Furthermore, LIF mitogenic action does not involve protein kinase C (PKC) activation, because a PKC inhibitor does not block this effect. In contrast, PKC activity is required for PGF2alpha mitogenic action. More importantly, the synergistic effect between LIF and PGF2alpha to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF- and PGF2alpha-dependent mechanism(s) that induce cellular entry into S phase. These findings are critical in understanding how LIF and other related cytokine-regulated events participate in normal cell cycle control and may also provide clues to unravel crucial processes underlying cancerous cell division.
publishDate 2006
dc.date.none.fl_str_mv 2006-03-10
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/11336/18518
Dekanty, Andres; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, Federico; Barrio, Marcela; et al.; Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation; American Society For Biochemistry And Molecular Biology; Journal Of Biological Chemistry; 28; 10; 10-3-2006; 6136-6143
0021-9258
CONICET Digital
CONICET
url http://hdl.handle.net/11336/18518
identifier_str_mv Dekanty, Andres; Sauane, Moira; Cárdenas, Belén; Coluccio Leskow, Federico; Barrio, Marcela; et al.; Leukaemia Inhibitory Factor (LIF) induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK 1/2 activation; American Society For Biochemistry And Molecular Biology; Journal Of Biological Chemistry; 28; 10; 10-3-2006; 6136-6143
0021-9258
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/281/10/6136.long
info:eu-repo/semantics/altIdentifier/doi/10.1074/jbc.M505839200
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 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
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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