Impairment of ATP-induced Ca super(2+)-signalling in human thyroid cancer cells
Extracellular nucleotides like ATP that activate the Ca super(2+)-phosphatidylinositol (PI) signalling pathway have been suggested to participate in the regulation of normal human thyroid function. We examined, whether P sub(2y)-purinergic receptors are expressed on human thyroid cancer cells and wh...
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Published in | Molecular and cellular endocrinology Vol. 133; no. 1; pp. 33 - 39 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
01.09.1997
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Abstract | Extracellular nucleotides like ATP that activate the Ca super(2+)-phosphatidylinositol (PI) signalling pathway have been suggested to participate in the regulation of normal human thyroid function. We examined, whether P sub(2y)-purinergic receptors are expressed on human thyroid cancer cells and whether post-receptor Ca super(2+) signalling is altered by malignant transformation. Extracellular ATP caused a biphasic increase in cytosolic free Ca super(2+) ([Ca super(2+)] sub(i)) in normal human thyrocytes and in human follicular (FTC) and papillary (PTC) thyroid carcinoma cells. In FTC and PTC cell lines the dose-response curves for ATP-induced changes in [Ca super(2+)] sub(i) were shifted to the right when compared with normal thyrocytes, whereas in undifferentiated thyroid carcinoma (UTC) cells even high concentrations of ATP (500 mu M) failed to stimulate a rise in [Ca super(2+)] sub(i). By contrast, ATP stimulated inositol 1,4,5-trisphosphate (IP sub(3)) formation and capacitative Ca super(2+) entry was operational as judged by thapsigargin in normal thyrocytes and all thyroid cancer cells. Thus, P sub(2y)-purinergic receptors are expressed on thyroid tumor cells independent of degree of differentiation. In UTC cells, however, impairment in the Ca super(2+)-phosphatidylinositol (PI) signalling cascade occurs distal to the formation of IP sub(3) and proximal to the activation of capacitative Ca super(2+) entry. Disturbed ATP-induced Ca super(2+)-signalling and alterations in the Ca super(2+)-PI signalling cascade may contribute to decreased expression or loss of specific thyroid functions in thyroid cancer cells. |
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AbstractList | Extracellular nucleotides like ATP that activate the Ca super(2+)-phosphatidylinositol (PI) signalling pathway have been suggested to participate in the regulation of normal human thyroid function. We examined, whether P sub(2y)-purinergic receptors are expressed on human thyroid cancer cells and whether post-receptor Ca super(2+) signalling is altered by malignant transformation. Extracellular ATP caused a biphasic increase in cytosolic free Ca super(2+) ([Ca super(2+)] sub(i)) in normal human thyrocytes and in human follicular (FTC) and papillary (PTC) thyroid carcinoma cells. In FTC and PTC cell lines the dose-response curves for ATP-induced changes in [Ca super(2+)] sub(i) were shifted to the right when compared with normal thyrocytes, whereas in undifferentiated thyroid carcinoma (UTC) cells even high concentrations of ATP (500 mu M) failed to stimulate a rise in [Ca super(2+)] sub(i). By contrast, ATP stimulated inositol 1,4,5-trisphosphate (IP sub(3)) formation and capacitative Ca super(2+) entry was operational as judged by thapsigargin in normal thyrocytes and all thyroid cancer cells. Thus, P sub(2y)-purinergic receptors are expressed on thyroid tumor cells independent of degree of differentiation. In UTC cells, however, impairment in the Ca super(2+)-phosphatidylinositol (PI) signalling cascade occurs distal to the formation of IP sub(3) and proximal to the activation of capacitative Ca super(2+) entry. Disturbed ATP-induced Ca super(2+)-signalling and alterations in the Ca super(2+)-PI signalling cascade may contribute to decreased expression or loss of specific thyroid functions in thyroid cancer cells. |
Author | Poetter, E Boerger, J Schoefl, C von zur Muehlen, A Roessig, L Brabant, G Mader, T |
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