Platelet-derived growth factor-stimulated c-myc RNA accumulation in MG-63 human osteosarcoma cells is independent of both protein kinase A and protein kinase C.

Frick, Kevin K.; Scher, Charles D.

doi:10.1128/mcb.10.1.184

Cited by 11 publications

(5 citation statements)

References 44 publications

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“…Only a few other studies have investigated the mechanism of the positive regulation of c-myc expression by CAMP. As in this work, a stimulatory effect of Fo on transcription has been observed in Swiss 3T3 (Kacich et al, 1988;Mehmet et al, 1988) and osteosarcoma (Frick and Scher, 1990) cell lines. c-myc is generally regulated at the transcriptional level by other mitogenic cascades and in other systems.…”

Section: Discussionsupporting

confidence: 60%

c-myc expression is controlled by the mitogenic cAMP-cascade in thyrocytes

Pirson¹,

Coulonval²,

Lamy³

et al. 1996

J. Cell. Physiol.

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In dog thyroid epithelial cells in primary culture, thyrotropin (TSH), acting through cAMP, induces proliferation and differentiation expression, whereas epidermal growth factor (EGF) and phorbol esters induce proliferation and dedifferentiation. In these cells, we have detailed the regulation by cAMP of the c-myc protooncogene mRNA and protein. The cAMP signaling pathway induces a biphasic increase of c-myc mRNA and protein. c-Myc protein accumulation follows the abundance and kinetics of its mRNA expression. Using in vitro elongation of nascent transcripts to measure transcription and actinomycin D (AcD) chase experiments to study mRNA stability, we have shown that in the first phase cAMP releases a transcriptional elongation block. No modification of transcriptional initiation was observed. After 30 min of treatment with TSH, c-myc mRNA was also stabilized. During the second phase, cAMP stabilization of the mRNA disappears and transcription is again shut off. Thus, in a tissue in which it stimulates proliferation and specific gene expression, cAMP regulates biphasically c-myc expression by mechanisms operating at the transcriptional and posttranscriptional levels.

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Section: Discussionsupporting

confidence: 60%

c-myc expression is controlled by the mitogenic cAMP-cascade in thyrocytes

Pirson¹,

Coulonval²,

Lamy³

et al. 1996

J. Cell. Physiol.

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“…In contrast to Egr-1, LPA was without effect on expression of c-Myc, a proto-oncogene. C-Myc may be abundantly expressed in human osteosarcoma [4] and is assumed to be upregulated in MG-63 cells after treatment with PDGF, forskolin and 12- O -tetradecanoylphorbol-13-acetate [66] .…”

Section: Discussionmentioning

confidence: 99%

LPA-induced suppression of periostin in human osteosarcoma cells is mediated by the LPA1/Egr-1 axis

et al. 2012

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Lysophosphatidic acid (LPA), a naturally occurring bioactive phospholipid, mediates a multitude of (patho)physiological events including activation of mitogen-activated protein kinases (MAPKs). As LPA may induce cellular reponses in human osteosarcoma, the present study aimed at investigating expression of various LPA receptors, LPA-mediated activation of MAPK via G-protein coupling, and expression of early response genes in a cellular model for human osteosarcoma. We show that MG-63 cells express three members of the endothelial differentiation gene (Edg) family of G-protein coupled receptor transcripts (LPA1–3) but only two (LPA4/5) out of three members of the non-Edg family LPA receptor transcripts. Stimulation of MG-63 cells with LPA or synthetic LPA receptor agonists resulted in p42/44 MAPK phosphorylation via LPA1–LPA3 receptors. Using pharmacological inhibitors, we show that LPA-mediated phosphorylation of p42/44 MAPK by LPA receptor engagement is transmitted by Gαi-dependent pathways through the Src family of tyrosine kinases. As a consequence, a rapid and transient upregulation of the zinc finger transcription factor early growth response-1 (Egr-1) was observed. Egr-1 expression was strictly mediated via Gαi/Src/p42/44 MAPK pathway; no involvement of the Gαq/11/PLC/PKC or the PLD/PI3 kinase/Akt pathways was found. LPA-induced expression of functional Egr-1 in MG-63 cells could be confirmed by electrophoretic mobility shift assay. LPA-induced Egr-1 upregulation was accompanied by a time-dependent decrease of periostin (previously called osteoblast-specific factor 2), a cell adhesion protein for pre-osteoblasts. Silencing of LPA1 and/or Egr-1 in MG-63 cells reversed LPA-mediated suppression of periostin. We here demonstrate a crosslink between Egr-1 and periostin in cancer cells, in particular in human osteosarcoma.

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“…Our data also showed that intracellular cAMP levels decreased in adult SCs treated with PDGF-BB. However, recent studies have indicated that PDGF treatment causes no alteration of CAMP in human FBs, MG-63 cells, or Swiss 3T3 cells (Heldin et al, 1989;Frick et al, 1990;Rozengurt et al, 1983). It is unclear what mechanism causes the decrease of cAMP in adult SCs in PDGF-BB treatment and whether this decrease is related to the fact that PDGF-BB dose not stimulate adult SCs proliferation.…”

Section: Discussionmentioning

confidence: 99%

Mitogn induced proliferation of isolated adult mouse schwann cells

Zhang

Hikawa

Horie

et al. 1995

J of Neuroscience Research

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The proliferation of neonatal Schwann cells (SCs) in response to mitogenic agents has been well analyzed in vitro, but a limited range of mitogens have been defined. We investigated whether three identified neonatal SC mitogens [glial growth factor (GGF), platelet-derived growth factor BB (PDGF-BB), and basic fibroblast growth factor (bFGF)] are required to stimulate mitosis of adult SCs. Adult SCs were isolated from mouse sciatic nerves by mechanical and chemical dissociation, following three experimental steps: 1) culturing the dissociated cells for 24 hr in 10% FCS-F12 medium, 2) culturing these cells in serum-free medium for the next 48 hr, and 3) purifying adult SCs by differential adhesion. We describe a new method for preparation of SCs from peripheral nerves of adult mouse that provides 99.5% pure SCs populations at cell yields of greater than 3 x 10(3) cells/mg of starting nerve wet weight within 5 culture days. Although mitosis of SCs in culture in response to mitogens requires the presence of serum, the complex nature of serum renders difficult a complete analysis of mitogens required for SCs DNA synthesis, so we examined the proliferating response of adult SCs to GGF, PDGF-BB, and bFGF in serum-free medium. GGF alone had mitogenicity for adult SCs in a dose-dependent manner, and synergistic activation coupling with forskolin was not observed. Neither PDGF-BB nor bFGF was mitogenic for adult SCs when used alone or with forskolin.(ABSTRACT TRUNCATED AT 250 WORDS)

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Platelet-derived growth factor-stimulated c-myc RNA accumulation in MG-63 human osteosarcoma cells is independent of both protein kinase A and protein kinase C.

Cited by 11 publications

References 44 publications

c-myc expression is controlled by the mitogenic cAMP-cascade in thyrocytes

c-myc expression is controlled by the mitogenic cAMP-cascade in thyrocytes

LPA-induced suppression of periostin in human osteosarcoma cells is mediated by the LPA1/Egr-1 axis

Mitogn induced proliferation of isolated adult mouse schwann cells

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