Leukaemia Inhibitory Factor Induces Mitogenesis in Swiss 3T3 Cells and Selective Enhancement via a Variety of Signalling Events

Levy, Carolina Schere; Sauane, Moira; Rudland, Philip S.; Asúa, Luis Jiménez de

doi:10.1006/bbrc.1997.7055

Cited by 6 publications

(10 citation statements)

References 28 publications

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“…7A, GF109203X progressively inhibited PGF 2␣ -dependent DNA replication but completely failed to block LIF-dependent DNA replication. These results are consistent with our previous findings obtained with 12-O-tetradecanoylphorbol-13-acetate indicating that LIF and PGF 2␣ differed markedly in the requirement for PKC in stimulating DNA synthesis (25). Most interestingly, GF109203X did not prevent the synergistic effect between PGF 2␣ and LIF in increasing the percentage of cells that entered into S phase (Fig.…”

Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 supporting

confidence: 93%

“…Cells were then labeled with [methyl-3 H]thymidine for 28 h before being processed for autoradiography. The percentage of cells that initiated DNA synthesis at a given time was determined as described previously (25,33).…”

Section: Methodsmentioning

confidence: 99%

“…The Synergistic Effect of LIF and PGF 2␣ to Induce S Phase Entry Is Independent of PKC Activation-We have shown previously that LIF and PGF 2␣ differ markedly in the requirement for PKC in stimulating DNA synthesis (25). LIF triggers cellular entry into S phase via a PKCindependent signaling mechanism, whereas PGF 2␣ requires the activation of the PKC signaling pathway (25).…”

Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 mentioning

confidence: 99%

“…LIF triggers cellular entry into S phase via a PKCindependent signaling mechanism, whereas PGF 2␣ requires the activation of the PKC signaling pathway (25). Therefore, we examined whether PGF 2␣ -dependent activation of PKC plays a role in the synergistic effect observed between LIF and PGF 2␣ in the induction of DNA synthesis in Swiss 3T3 cells.…”

Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 mentioning

confidence: 99%

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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

Sauane

Cadenas

et al. 2006

Journal of Biological Chemistry

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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 2␣ (PGF 2␣ ) occurs, in part, through different signaling events. LIF and OSM specifically trigger STAT1 cytoplasmic to nuclear translocation, whereas PGF 2␣ fails to do so. However, LIF and PGF 2␣ 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 2␣ treatment. PGF 2␣ 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 2␣ 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 2␣ mitogenic action. More importantly, the synergistic effect between LIF and PGF 2␣ to promote S phase entry is independent of PKC activation. These results show fundamental differences between LIF-and PGF 2␣ -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. Leukemia inhibitory factor (LIF)5 belongs to a closely related group of cytokines, which includes oncostatin M (OSM), ciliary neurotrophic factor (CNTF), interleukin 6 (IL-6), and cardiotrophin-1 (1-4).Depending on the cell type, LIF promotes cellular proliferation or differentiation, e.g. embryonic stem cell growth (5, 6), mammalian embryo implantation (2, 4), neuronal differentiation (7, 8), enhancing survival of peripheral neurons (7) and oligodendrocytes (10), promoting bone formation (11), and myoblast proliferation (12)(13)(14). LIF is also implicated in a variety of pathophysiological processes (15)(16)(17)(18)(19). Cellular responses to LIF as well as to other cytokines are initiated via heterodimerization of two members of the cytokine receptor family (8,20,21). The resultant signal transduction process involves activation of cytoplasmic Janus kinases (8, 20, 21), which in turn promote tyrosine phosphorylation of the signal transducers and activators of transcription (STATs), thereby enabling them to translocate to the nucleus and initiate gene transcription of LIF-responsive genes (22). LIF can also trigger alternative signaling processes to those causing STAT activation (23). These include activation of the mitogen-activated protein kinase (MAPK) cascade, including the mitogen-activated protei...

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Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 supporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 mentioning

confidence: 99%

Section: D Lif Did Not Promote Full Phosphorylation Of Prb (Lane 4 mentioning

confidence: 99%

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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

Sauane

Cadenas

et al. 2006

Journal of Biological Chemistry

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“…Briefly, 1.5 · 10 5 cells were seeded in 35 mm dishes and growth until confluent and quiescent (6-8 days H] thymidine for 28 h and processed for autoradiography. The percentage of cells that initiated DNA synthesis at a given time was determined as previously described [4,16].…”

Section: Initiation Of Dna Synthesis Assaymentioning

confidence: 99%

Differential involvement of ERK_1‐2 and p38^MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F_2α

et al. 2006

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Prostaglandin F 2a (PGF 2a ) induces cyclin D 1 expression and DNA synthesis in Swiss 3T3 cells. In order to assess which signaling mechanisms are implicated in these processes, we have used both a pharmacological approach and interfering mutants. We demonstrate that PGF 2a induces extracellular-signal-regulated kinase (ERK 1-2 ) and p38MAPK activation, and inhibition of any of these signaling pathways completely blocks PGF 2a -stimulated DNA synthesis. We also show that ERK 1-2 , but not p38 MAPK activation is required to induce cyclin D 1 expression, strongly suggesting that the concerted action of cyclin D 1 gene expression and other events are required to induce complete phosphorylation of retinoblastoma protein and S-phase entry in response to PGF 2a .

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Prostaglandin F2α (PGF2α) Induces Cyclin D1 Expression and DNA Synthesis via Early Signaling Mechanisms in Swiss Mouse 3T3 Cells

Sauane

Corrêa

Rogers

et al. 2000

Biochemical and Biophysical Research Communications

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Leukaemia Inhibitory Factor Induces Mitogenesis in Swiss 3T3 Cells and Selective Enhancement via a Variety of Signalling Events

Cited by 6 publications

References 28 publications

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 Induces DNA Synthesis in Swiss Mouse 3T3 Cells Independently of Cyclin D1 Expression through a Mechanism Involving MEK/ERK1/2 Activation

Differential involvement of ERK_1‐2 and p38^MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F_2α

Prostaglandin F2α (PGF2α) Induces Cyclin D1 Expression and DNA Synthesis via Early Signaling Mechanisms in Swiss Mouse 3T3 Cells

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Leukaemia Inhibitory Factor Induces Mitogenesis in Swiss 3T3 Cells and Selective Enhancement via a Variety of Signalling Events

Cited by 6 publications

References 28 publications

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 Induces DNA Synthesis in Swiss Mouse 3T3 Cells Independently of Cyclin D1 Expression through a Mechanism Involving MEK/ERK1/2 Activation

Differential involvement of ERK1‐2 and p38MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F2α

Prostaglandin F2α (PGF2α) Induces Cyclin D1 Expression and DNA Synthesis via Early Signaling Mechanisms in Swiss Mouse 3T3 Cells

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Differential involvement of ERK_1‐2 and p38^MAPK activation on Swiss 3T3 cell proliferation induced by prostaglandin F_2α