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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/18518
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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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1842268593713053696 |
score |
13.13397 |