Serum Factors Inhibit Melanoma Cell Surface Expression of Type I and Type II IGF Receptors

Bellan, Catherine; Remacle‐Bonnet, Maryse; Garrouste, Françoise; Secchi, J.; Luis, José; Pommier, Gilbert; Marvaldi, Jacques

doi:10.3109/10799899609039944

Cited by 2 publications

(2 citation statements)

References 24 publications

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“…The possibility that the lack of effects of CH-275 on [Ca 2+ ] i is due to an altered sst 1 receptor expression can be excluded by the finding that GC cells express sst 1 receptors irrespective of their culture conditions. Indeed, different culture conditions are known to influence protein expression in various cell types [33, 34, 35]. Another possibility is the difference in time scales of CH-275 application used for [Ca 2+ ] i measurements and GH experiments.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Control of Growth Hormone Secretion by Somatostatin in Rat Pituitary GC Cells: sst2 but Not sst1 Receptors Are Coupled to Inhibition of Single-Cell Intracellular Free Calcium Concentrations

Cervia

Petrucci²,

Bluet-Pajot³

et al. 2002

Neuroendocrinology

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Rat pituitary tumor cells (GC cells) exhibit spontaneous oscillations of intracellular free calcium concentration ([Ca²⁺]_i) that allow continuous release of growth hormone (GH). Of the somatostatin (SRIH) receptor subtypes (sst receptors) mediating SRIH action, sst₁ and sst₂ receptors are highly expressed by GC cell membranes. In the present study, the effects of sst₁ or sst₂ receptor activation on single-cell [Ca²⁺]_i were investigated in GC cells by confocal fluorescence microscopy. In addition, the effects of sst₁ or sst₂ receptor activation on GH secretion were also studied. Our results demonstrate that SRIH decreases [Ca²⁺]_i baseline and almost completely blocks Ca²⁺ transients through activation of sst₂ but not of sst₁ receptors. In contrast, SRIH effectively inhibits GH secretion through activation of both sst₁ and sst₂ receptors. Blocking Ca²⁺ transients is less efficient than SRIH to inhibit GH release. The cyclic octapeptide, CYN-154806, antagonizes sst₂ receptors at [Ca²⁺]_i since it abolishes the sst₂ receptor-mediated inhibition of [Ca²⁺]_i without affecting single-cell Ca²⁺ signals. On the other hand, CYN-154806 alone potently inhibits GH secretion through the involvement of pertussis toxin-sensitive G proteins. In conclusion, the present results demonstrate that SRIH inhibition of GH release in GC cells involves mechanisms either dependent or independent on SRIH modulation of [Ca²⁺]_i. The implications of CYN-154806 inhibition of GH secretion are discussed.

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Section: Discussionmentioning

confidence: 99%

Inhibitory Control of Growth Hormone Secretion by Somatostatin in Rat Pituitary GC Cells: sst2 but Not sst1 Receptors Are Coupled to Inhibition of Single-Cell Intracellular Free Calcium Concentrations

Cervia

Petrucci²,

Bluet-Pajot³

et al. 2002

Neuroendocrinology

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“…IGF-I is a primary mitogen for a number of malignant melanoma cell lines (45). Studies on melanoma cell lines (46,47) indicate synthesis of a range of IGFBPs (IGFBP-2, -3, -4, -5, and -6), with regulation by serum or IGF-I. It is thus possible that aberrantly expressed IGFBPs play a more significant role in regulating the IGF-I response of melanoma cells.…”

Section: Discussionmentioning

confidence: 99%

Interactions between Growth Hormone, Insulin-Like Growth Factor I, and Basic Fibroblast Growth Factor in Melanocyte Growth1

Edmondson

Russo

McFARLANE

et al. 1999

The Journal of Clinical Endocrinology &Amp; Metabolism

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Melanocytes, highly differentiated neural crest-derived cells, are located in the basal layer of the epidermis, where they play a role in protecting against UV damage in the skin. Previous studies suggest that both growth hormone (GH) and the insulin-like growth factor I (GH/IGF-I) system may be important for melanocyte growth and function. We have therefore characterized the role of the GH/IGF system in melanocyte growth in vitro and its interaction with the local growth factor basic fibroblast growth factor (bFGF). Analysis of the effects of GH, IGF-I, and bFGF and combinations of these growth factors on melanocyte growth in vitro revealed that 1) GH stimulates the growth of melanocytes when combined with IGF-I, des(1-3)IGF-I [an analog of IGF-I that has a reduced binding affinity for IGF-binding proteins (IGFBPs)], or bFGF, either separately or in combination; 2) in contrast to the lack of effect of GH or bFGF alone, both IGF-I and des(1-3)IGF-I enhance melanocyte growth in a dose-dependent manner; and 3) IGF-I is more efficacious in eliciting a growth response at low concentrations compared to des(1-3)IGF-I. Using Western ligand blotting, affinity cross-linking, immunoprecipitation, RIA, and Northern analysis, we show that cultured human melanocytes synthesize and secrete minimal amounts of IGFBP. IGFBP-4 is the major IGFBP produced by these cells when cultured in complete growth medium or in the presence of either IGF-I or des(1-3)IGF-I alone. In conclusion, these studies provide support for a role for both GH and IGF-I in the growth of human melanocytes in vitro, involving synergy with bFGF. Low levels of melanocyte-derived IGFBP-4 may play a role in enhancing the modulation of IGF action.

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Serum Factors Inhibit Melanoma Cell Surface Expression of Type I and Type II IGF Receptors

Cited by 2 publications

References 24 publications

Inhibitory Control of Growth Hormone Secretion by Somatostatin in Rat Pituitary GC Cells: sst<sub>2</sub> but Not sst<sub>1</sub> Receptors Are Coupled to Inhibition of Single-Cell Intracellular Free Calcium Concentrations

Inhibitory Control of Growth Hormone Secretion by Somatostatin in Rat Pituitary GC Cells: sst<sub>2</sub> but Not sst<sub>1</sub> Receptors Are Coupled to Inhibition of Single-Cell Intracellular Free Calcium Concentrations

Interactions between Growth Hormone, Insulin-Like Growth Factor I, and Basic Fibroblast Growth Factor in Melanocyte Growth1

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