Defective thyrotropin receptor G-protein cyclic adenosine monophosphate signaling mechanism in the FTC human follicular thyroid cancer cell line

Surgery
M J DemeureS D Wilson

Abstract

Several studies report the effect of thyrotropin (thyroid-stimulating hormone [TSH]) on FTC-133) and aggressively invasive (FTC-238) clones of a human follicular thyroid cancer cell line. Specifically, TSH induces fibronectin secretion by FTC-133, possibly as a result of increased cyclic adenosine monophosphate (cAMP), yet induces in vitro invasion through a protein kinase C-dependent mechanism. In normal thyrocytes, TSH activates cAMP through a stimulatory G-protein (Gs)-linked pathway. In the FTC model we studied the effect of TSH on adenylate cyclase activation. TSH receptor (TSH-R) mRNA was studied by reverse transcriptase polymerase chain reaction. Fibronectin transcription was analyzed by Northern blot and densitometry. cAMP levels were determined by an enzyme immunoassay. Gs alpha expression was determined by Western blot and a possible activating mutation at position 201 in Gs alpha sought by direct sequencing. Reverse transcriptase polymerase chain reaction confirmed the presence of TSH-R mRNA in FTC-133 and FTC-238. TSH did not increase transcription of fibronectin mRNA. FTC-133 cells exhibited higher cAMP levels than did FTC-238 cells: 30.4 +/- 8.0 versus 13.0 +/- 3.5 femtomoles/10(4) cells (mean +/- SD; p < 0.001, M...Continue Reading

References

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Sep 30, 1993·Biochemical and Biophysical Research Communications·T HoeltingO H Clark

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Citations

Dec 25, 2008·European Journal of Nuclear Medicine and Molecular Imaging·Eleonore FröhlichRichard Wahl
Nov 19, 2008·Thyroid : Official Journal of the American Thyroid Association·Eleonore FröhlichRichard Wahl
May 1, 2008·The Journal of Biological Chemistry·Thomas R H BüchThomas Gudermann

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