Differential Protein Phosphorylation in Induction of Thyroid Cell Proliferation by Thyrotropin, Epidermal Growth Factor, or Phorbol Ester

Contor, Laura S.; Lamy, Françoise; Lecocq, Raymond; Roger, Pierre P.; Dumont, Jacques Emile

doi:10.1128/mcb.8.6.2494-2503.1988

Cited by 2 publications

(2 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effect of EGF on thyroid cells is probably mediated through its tyrosine kinase activity and stimulation of phosphatidylinositol (PI) turnover. PI turnover causes an elevation of inositol 1,4,5-triphosphate (IP3) production with increase in intracellular calcium [25], and cytoplasmic alkalization (in pig thyroid) [26], and increased 1,2-diacylglycerol (DAG) with activation of protein kinase C (in dog thyroid) [27]. EGF stimulates the expression of c-fos and c-myc oncogenes, while TSH has no such effect in the cell culture of the pig thyroid [28].…”

Section: Egf Stimulates Thyroid Growthmentioning

confidence: 99%

Epidermal growth factor receptors and adenylate cyclase activity in human thyroid tissues

et al. 1990

View full text Add to dashboard Cite

Thyroid stimulating hormone (TSH) and epidermal growth factor (EGF) are growth factors for some thyroid cells in cultures. We have previously found more EGF receptors in neoplastic human thyroid tissues than in normal thyroid tissues. We have also found a higher TSH-stimulated adenylate cyclase (AC) activity in neoplastic human thyroid tissues than in normal thyroid tissues. To clarify the relationship between the effect of EGF and TSH on thyroid tissue, we measured the binding of EGF and TSH and the basal, TSH-stimulated and forskolin-stimulated adenylate cyclase activity in 49 normal, hyperplastic and neoplastic human thyroid tissues (5 normal, 2 Hashimoto thyroiditis, 5 Graves' disease, 14 multinodular goiters, 9 follicular adenomas, 5 follicular carcinomas, 8 papillary carcinomas, and 1 undifferentiated carcinoma). Specific binding of EGF and TSH were measured by radioreceptor assays using competitive inhibition of radio-labeled ligand by unlabeled ligand. Basal, maximally (300 mU/ml) TSH-stimulated, and maximally (100 mM) forskolin-stimulated adenylate cyclase activities were also measured in the same membrane particulate fractions from the thyroid tissues. We found: neoplastic thyroid tissues bind more labeled EGF than nonneoplastic thyroid tissues; follicular adenomas and carcinomas have higher EGF binding than other thyroid tissues; a weak but significant correlation between specific EGF binding and specific TSH binding, and between specific EGF binding and TSH-stimulated adenylate cyclase activity of the thyroid membrane preparations. These findings are consistent with the hypothesis that TSH stimulates an increase in thyroid EGF receptors by increasing intracellular cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: Egf Stimulates Thyroid Growthmentioning

confidence: 99%

Epidermal growth factor receptors and adenylate cyclase activity in human thyroid tissues

et al. 1990

View full text Add to dashboard Cite

show abstract

“…The tumor promoter TPA is a potent promoter of thyroid proliferation and increases PKC activity [13][14][15]. Roger et al [16] documented that TPA induced DNA synthesis and proliferation of dog thyroid cells.…”

mentioning

confidence: 99%

Heterologous Desensitization in Neoplastic Thyroid Cells: Influence of the Phospholipase C Signal Transduction System on the Thyrotropin–adenylate Cyclase Signal Transduction System

Tezelman

Hoelting

Jossart³

et al. 1998

World j. surg.

View full text Add to dashboard Cite

Desensitization is defined as a decreased functional response after continuous or repetitive stimulation of a receptor with its agonist. Thyrotropin (TSH) increases cAMP levels in normal and neoplastic thyroid tissue. The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) activates protein kinase C (PKC). The aim was to determine whether TPA induces heterologous desensitization of the TSH-adenylate cyclase (AC) signal transduction system. Three human thyroid neoplasms in culture for 6 months or longer (one papillary carcinoma, one Hurthle cell carcinoma, one follicular adenoma) were incubated with TSH (10 mU/ml) and TPA (1.6 x 10(-8) M) separately and together for various time periods (from 10 minutes to 24 hours). The mixture was subsequently incubated for 30 minutes with TSH. TPA alone had no effect on cAMP levels, but co-incubation of TPA and TSH caused a significant reduction in cAMP response when compared to the cAMP response that resulted after stimulation with only TSH (p < 0.001). cAMP levels in response to TSH decreased by 31%, 44%, and 57% after preincubation with TSH for 10 minutes, 4 hours, and 24 hours, respectively (p < 0.01; ANOVA). Co-incubation of cells with TPA and staurosporine (10 ng/ml), a PKC inhibitor, prevented the effect of TPA on desensitization at 10 minutes and blunted the effect at 4 hours. This is the first demonstration in human neoplastic thyroid cells that TPA induced heterologous desensitization of the cAMP response to TSH. This TPA-induced effect appears to involve PKC activation, as it can be blocked by staurosporine.

show abstract

Differential Protein Phosphorylation in Induction of Thyroid Cell Proliferation by Thyrotropin, Epidermal Growth Factor, or Phorbol Ester

Cited by 2 publications

References 38 publications

Epidermal growth factor receptors and adenylate cyclase activity in human thyroid tissues

Epidermal growth factor receptors and adenylate cyclase activity in human thyroid tissues

Heterologous Desensitization in Neoplastic Thyroid Cells: Influence of the Phospholipase C Signal Transduction System on the Thyrotropin–adenylate Cyclase Signal Transduction System

Contact Info

Product

Resources

About