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

Sauane, Moira; Corrêa, Laura Trevizan; Rogers, Florencia; Krasnapolski, Martín; Barraclough, Roger; Rudland, Philip S.; Asúa, Luis Jiménez de

doi:10.1006/bbrc.2000.2383

Cited by 9 publications

(14 citation statements)

References 32 publications

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“…These findings agree with the early S-phase arrest found in 3T6 fibroblasts after AH-23848B treatment that may result from the decrease in cyclin A levels. Previous studies have shown that PGF 2␣ induced cyclin D1 expression and DNA synthesis in 3T3 cells (44), but to our knowledge this is the first report on PGE 2 controlling progression through different phases of the cell cycle by interacting with two different subtype receptors.…”

Section: Discussionmentioning

confidence: 69%

Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Sánchez

2002

American Journal of Physiology-Cell Physiology

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Recent studies have suggested that prostaglandin E2 (PGE2) subtype receptors (EP) are involved in cellular proliferation and tumor development. We studied the role of EP1 and EP4 PGE2 subtype receptor antagonists AH-6809 and AH-23848B, respectively, in serum-induced 3T6 fibroblast proliferation. This was significantly reduced in a dose-dependent manner (IC50 ϳ100 and ϳ30 M, respectively) to an almost complete inhibition, without any cytotoxic effect. However, the effect of each antagonist on 3T6 cell cycle progression clearly differed. Whereas the EP1 antagonist increased the G0/G1 population, the EP4 antagonist brought about an accumulation of cells in early S phase. These effects were associated with a decrease in cyclin D and E levels in AH-6809-treated 3T6 cells and lower cyclin A levels in AH-23848B-treated fibroblasts with respect to control cells. The G0/G1 accumulation caused by AH-6809 seems to be intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) dependent, because a 6-h 1 M thapsigargin treatment allowed G 0/G1-arrested cells to enter S phase. Similarly, treatment with 20 M forskolin for 6 h allowed S-phase and G 2/M progression of AH-23848B-treated cells. This study shows that the inhibitory effect of the EP 1 and EP4 antagonists on serum-induced 3T6 fibroblast growth is due to their effect at various levels of the cell cycle machinery, suggesting that PGE 2 interaction with its different subtype receptors regulates progression through the cell cycle by modulating cAMP and [Ca 2ϩ ]i. arachidonic acid; cyclooxygenase; prostaglandin G/H synthase; phospholipase A 2

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Section: Discussionmentioning

confidence: 69%

Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Sánchez

2002

American Journal of Physiology-Cell Physiology

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“…Thus, cyclin D1 expression and S-phase entry were induced by prostaglandin F2α in Swiss 3T3 fibroblasts, whereas other prostaglandins were able to arrest cells at the G2/M phase of the cell cycle. 49,50 We have shown that cPLA 2 activity increased transiently during mid-G1 phase of the ongoing cell cycle of CHO and neuroblastoma N2A cells, this activity being dependent upon the activity of p42/44. 51,52 By using different inhibitors of cPLA 2 , it was demonstrated that the activity of cPLA 2 in mid-G1 phase was required for entry into S phase.…”

Section: A the Map Kinase Pathwaymentioning

confidence: 94%

Signal Transduction and Actin in the Regulation of G1-Phase Progression

Boonstra

Moes

2005

Crit Rev Eukar Gene Expr

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Regulation of cell proliferation is dependent on the integration of signal transduction systems that are activated by external signal molecules, such as growth factors and extracellular matrix components. Dependent on these signal transduction networks, the cells decide in the G1 phase to continue proliferation or, alternatively, to stop cell-cycle progression and undergo apoptosis, differentiation, or quiescence. The MAP kinase and PI-3 kinase pathways have been demonstrated to play an essential role in these G1-phase decisions. Interestingly, actin has been demonstrated to mutually interfere with signal transduction. In addition, it has been indicated that the FOXO transcription factors are involved in these decisions, as well. Actin has been demonstrated to play an important role in the regulation of G1-phase progression. Because of its properties as a structural protein, actin is essential in cytokinesis and in cell spreading and, thus, is involved in G1-phase progression. As an intermediate factor in signal transduction, actin is likely to be involved in cell-cycle regulation induced by external signal molecules. And, finally, actin has been demonstrated to play a direct role in transcription. These observations indicate a prominent role of actin in the regulation of G1-phase progression.

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“…Protein extracts were prepared as in Sauane et al [14]. Fifty micrograms of protein were separated on SDS-polyacrylamide gels and blotted onto nitrocellulose membranes.…”

Section: Sds-page and Immunoblottingmentioning

confidence: 99%

“…PGF 2a -stimulation of DNA synthesis in Swiss 3T3 cells also requires PKC activation [14], and PKC activation has been shown to be one of the possible pathways leading to ERK 1-2 activation [20]. Thus, to determine whether PGF 2a -triggered ERK 1-2 activation is a downstream event of PKC activation, we used a specific PKC inhibitor (GF109203X).…”

Section: Erk 1-2 and P38mentioning

confidence: 99%

“…Such a PKC-independent process may correspond to other early PGF 2a -triggered events and both PKC-dependent and independent signals appear to be concertedly required for cells to initiate DNA synthesis. Furthermore, PGF 2a appears to induce DNA synthesis via the combined actions of the induction of cyclin D 1 gene expression and other signaling pathway-triggered events [14]. Thus, a basic question regarding PGF 2a signaling mechanisms is whether, and how, each personalized PGF 2a signal regulates cyclin D 1 expression, and how such events and others can ultimately control initiation of DNA synthesis.…”

Section: Introductionmentioning

confidence: 99%

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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

Cited by 9 publications

References 32 publications

Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Signal Transduction and Actin in the Regulation of G1-Phase Progression

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

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

Cited by 9 publications

References 32 publications

Role of EP1and EP4PGE2subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Role of EP1and EP4PGE2subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Signal Transduction and Actin in the Regulation of G1-Phase Progression

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

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Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

Role of EP₁and EP₄PGE₂subtype receptors in serum-induced 3T6 fibroblast cycle progression and proliferation

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