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首页> 外文期刊>Life sciences >Excessive activation of tyrosine kinases leads to inhibition of proliferation in a thyroid carcinoma cell line.
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Excessive activation of tyrosine kinases leads to inhibition of proliferation in a thyroid carcinoma cell line.

机译：酪氨酸激酶的过度活化导致抑制甲状腺癌细胞系中的增殖。

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Autocrine stimulation of growth is a hallmark of many tumor cell lines. In this work we investigated the synthesis and secretion of growth factors and the expression of their corresponding receptors in HTC-TSHr thyroid carcinoma cells. These cells synthesize epidermal growth factor (EGF) receptors and platelet-derived growth factor beta (PDGF beta) receptors and in addition transforming growth factor alpha (TGF alpha), PDGF-A and PDGF-B chains, respectively. Addition of EGF or PDGF-BB to the culture medium resulted in growth inhibition of HTC-TSHr cells. In contrast, treatment of the cells with low concentrations of neutralizing anti-TGF alpha antibodies or tyrosine kinase inhibitors led to stimulation of cell proliferation. Low concentrations of neutralizing anti-PDGF-B antibodies did not affect growth of the cells. As expected, cell proliferation was inhibited when high concentrations of either neutralizing anti-TGF alpha antibodies or anti-PDGF-B antibodies were applied. PDGF-AA did not influence growth of HTC-TSHr cells. We conclude that growth of HTC-TSHr thyroid carcinoma cells is influenced by two autocrine loops between TGF alpha and EGF receptors and between PDGF-B and PDGF beta receptors. However, our data suggest that excessive activation of tyrosine kinase receptors in these cells results in a relative inhibition rather than stimulation of growth.
机译：自分泌刺激生长是许多肿瘤细胞系的标志。在这项工作中，我们研究了HTC-TSHr甲状腺癌细胞中生长因子的合成和分泌及其相应受体的表达。这些细胞合成表皮生长因子（EGF）受体和血小板衍生的生长因子β（PDGFβ）受体，此外还分别转化转化生长因子α（TGFα），PDGF-A和PDGF-B链。将EGF或PDGF-BB添加至培养基导致HTC-TSHr细胞的生长抑制。相反，用低浓度的中和性抗TGFα抗体或酪氨酸激酶抑制剂处理细胞会刺激细胞增殖。低浓度的中和性抗PDGF-B抗体不会影响细胞的生长。如预期的那样，当应用高浓度的中和性抗TGFα抗体或抗PDGF-B抗体时，细胞增殖受到抑制。 PDGF-AA不影响HTC-TSHr细胞的生长。我们得出结论，HTC-TSHr甲状腺癌细胞的生长受到TGFα和EGF受体之间以及PDGF-B和PDGFβ受体之间的两个自分泌环的影响。但是，我们的数据表明，这些细胞中酪氨酸激酶受体的过度活化导致相对抑制而不是刺激生长。

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