Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation
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 prostaglandi...
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| Autores principales: | , , , , , |
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| Publicado: |
2006
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| Acceso en línea: | https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v281_n10_p6136_Dekanty http://hdl.handle.net/20.500.12110/paper_00219258_v281_n10_p6136_Dekanty |
| Aporte de: |
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paper:paper_00219258_v281_n10_p6136_Dekanty |
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dspace |
| institution |
Universidad de Buenos Aires |
| institution_str |
I-28 |
| repository_str |
R-134 |
| collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
| topic |
Leukemia Phosphorylation Translocation Biosynthesis Cells Cytology Diseases Enzyme inhibition DNA cyclin D cyclin D1 cyclin E leukemia inhibitory factor messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase kinase 1 STAT1 protein uo 126 cyclin G cycline cytokine interleukin 6 leukemia inhibitory factor Lif protein, mouse mitogen activated protein kinase mitogen activated protein kinase kinase oncostatin M Osm protein, mouse prostaglandin F2 alpha protein kinase C protein tyrosine kinase retinoblastoma protein STAT protein animal cell animal tissue article cell cycle cell cycle S phase cell division cell strain 3T3 controlled study DNA replication DNA synthesis mitogenesis mouse nonhuman phosphorylation priority journal protein analysis protein expression protein function protein induction retinoblastoma signal transduction animal biosynthesis DNA replication enzyme activation genetics kinetics metabolism physiology Animals Cyclin D1 Cyclins Cytokines Dinoprost DNA Replication Enzyme Activation Extracellular Signal-Regulated MAP Kinases Interleukin-6 Kinetics Leukemia Inhibitory Factor Mice Mitogen-Activated Protein Kinase Kinases Oncostatin M Phosphorylation Protein Kinase C Protein-Tyrosine Kinases Retinoblastoma Protein S Phase Signal Transduction STAT Transcription Factors Swiss 3T3 Cells |
| spellingShingle |
Leukemia Phosphorylation Translocation Biosynthesis Cells Cytology Diseases Enzyme inhibition DNA cyclin D cyclin D1 cyclin E leukemia inhibitory factor messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase kinase 1 STAT1 protein uo 126 cyclin G cycline cytokine interleukin 6 leukemia inhibitory factor Lif protein, mouse mitogen activated protein kinase mitogen activated protein kinase kinase oncostatin M Osm protein, mouse prostaglandin F2 alpha protein kinase C protein tyrosine kinase retinoblastoma protein STAT protein animal cell animal tissue article cell cycle cell cycle S phase cell division cell strain 3T3 controlled study DNA replication DNA synthesis mitogenesis mouse nonhuman phosphorylation priority journal protein analysis protein expression protein function protein induction retinoblastoma signal transduction animal biosynthesis DNA replication enzyme activation genetics kinetics metabolism physiology Animals Cyclin D1 Cyclins Cytokines Dinoprost DNA Replication Enzyme Activation Extracellular Signal-Regulated MAP Kinases Interleukin-6 Kinetics Leukemia Inhibitory Factor Mice Mitogen-Activated Protein Kinase Kinases Oncostatin M Phosphorylation Protein Kinase C Protein-Tyrosine Kinases Retinoblastoma Protein S Phase Signal Transduction STAT Transcription Factors Swiss 3T3 Cells Dekanty, Andrés Sauane, Moira Cadenas, María Belén Barrio, María Marcela Coso, Omar Adrian Jiménez de Asúa, Luis A.F. Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| topic_facet |
Leukemia Phosphorylation Translocation Biosynthesis Cells Cytology Diseases Enzyme inhibition DNA cyclin D cyclin D1 cyclin E leukemia inhibitory factor messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase kinase 1 STAT1 protein uo 126 cyclin G cycline cytokine interleukin 6 leukemia inhibitory factor Lif protein, mouse mitogen activated protein kinase mitogen activated protein kinase kinase oncostatin M Osm protein, mouse prostaglandin F2 alpha protein kinase C protein tyrosine kinase retinoblastoma protein STAT protein animal cell animal tissue article cell cycle cell cycle S phase cell division cell strain 3T3 controlled study DNA replication DNA synthesis mitogenesis mouse nonhuman phosphorylation priority journal protein analysis protein expression protein function protein induction retinoblastoma signal transduction animal biosynthesis DNA replication enzyme activation genetics kinetics metabolism physiology Animals Cyclin D1 Cyclins Cytokines Dinoprost DNA Replication Enzyme Activation Extracellular Signal-Regulated MAP Kinases Interleukin-6 Kinetics Leukemia Inhibitory Factor Mice Mitogen-Activated Protein Kinase Kinases Oncostatin M Phosphorylation Protein Kinase C Protein-Tyrosine Kinases Retinoblastoma Protein S Phase Signal Transduction STAT Transcription Factors Swiss 3T3 Cells |
| 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 F 2α (PGF 2α) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF 2α fails to do so. However, LIF and PGF 2α 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 PGF 2α treatment. PGF 2α 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 PGF 2α 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 PGF 2α mitogenic action. More importantly, the synergistic effect between LIF and PGF 2α to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF and PGF 2α-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. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc. |
| author |
Dekanty, Andrés Sauane, Moira Cadenas, María Belén Barrio, María Marcela Coso, Omar Adrian Jiménez de Asúa, Luis A.F. |
| author_facet |
Dekanty, Andrés Sauane, Moira Cadenas, María Belén Barrio, María Marcela Coso, Omar Adrian Jiménez de Asúa, Luis A.F. |
| author_sort |
Dekanty, Andrés |
| title |
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| title_short |
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| title_full |
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| title_fullStr |
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| title_full_unstemmed |
Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation |
| title_sort |
leukemia inhibitory factor induces dna synthesis in swiss mouse 3t3 cells independently of cyclin d1 expression through a mechanism involving mek/erk1/2 activation |
| publishDate |
2006 |
| url |
https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v281_n10_p6136_Dekanty http://hdl.handle.net/20.500.12110/paper_00219258_v281_n10_p6136_Dekanty |
| work_keys_str_mv |
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| _version_ |
1768544440956223488 |
| spelling |
paper:paper_00219258_v281_n10_p6136_Dekanty2023-06-08T14:43:27Z Leukemia inhibitory factor induces DNA synthesis in Swiss mouse 3T3 cells independently of cyclin D1 expression through a mechanism involving MEK/ERK1/2 activation Dekanty, Andrés Sauane, Moira Cadenas, María Belén Barrio, María Marcela Coso, Omar Adrian Jiménez de Asúa, Luis A.F. Leukemia Phosphorylation Translocation Biosynthesis Cells Cytology Diseases Enzyme inhibition DNA cyclin D cyclin D1 cyclin E leukemia inhibitory factor messenger RNA mitogen activated protein kinase 1 mitogen activated protein kinase 3 mitogen activated protein kinase kinase 1 STAT1 protein uo 126 cyclin G cycline cytokine interleukin 6 leukemia inhibitory factor Lif protein, mouse mitogen activated protein kinase mitogen activated protein kinase kinase oncostatin M Osm protein, mouse prostaglandin F2 alpha protein kinase C protein tyrosine kinase retinoblastoma protein STAT protein animal cell animal tissue article cell cycle cell cycle S phase cell division cell strain 3T3 controlled study DNA replication DNA synthesis mitogenesis mouse nonhuman phosphorylation priority journal protein analysis protein expression protein function protein induction retinoblastoma signal transduction animal biosynthesis DNA replication enzyme activation genetics kinetics metabolism physiology Animals Cyclin D1 Cyclins Cytokines Dinoprost DNA Replication Enzyme Activation Extracellular Signal-Regulated MAP Kinases Interleukin-6 Kinetics Leukemia Inhibitory Factor Mice Mitogen-Activated Protein Kinase Kinases Oncostatin M Phosphorylation Protein Kinase C Protein-Tyrosine Kinases Retinoblastoma Protein S Phase Signal Transduction STAT Transcription Factors Swiss 3T3 Cells 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 F 2α (PGF 2α) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF 2α fails to do so. However, LIF and PGF 2α 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 PGF 2α treatment. PGF 2α 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 PGF 2α 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 PGF 2α mitogenic action. More importantly, the synergistic effect between LIF and PGF 2α to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF and PGF 2α-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. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc. Fil:Dekanty, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Sauane, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Cadenas, B. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Barrio, M. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Coso, O.A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Jiménez De Asúa, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. 2006 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v281_n10_p6136_Dekanty http://hdl.handle.net/20.500.12110/paper_00219258_v281_n10_p6136_Dekanty |