Insulin‐and insulin‐like growth‐factor‐I receptor tyrosine‐kinase activities in human renal carcinoma
Insulin‐and insulin‐like growth‐factor‐I receptor tyrosine‐kinase activities in human renal carcinoma
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人肾癌中胰岛素和胰岛素样生长因子 I 受体酪氨酸激酶活性
DOI：
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发表时间：
1995
影响因子：
6.4
通讯作者：
H. Häring
中科院分区：
文献类型：
--
作者：
M. Kellerer;H. von Eye Corleta;Andreas Mühlhöfer;E. Capp;L. Mosthaf;S. Bock;P. Petrides;H. Häring
我们研究了人肾癌中胰岛素和胰岛素样生长因子1（IGF-1）受体的表达和功能特征。在8名成人患者的肾癌和正常邻近肾组织中分析了两种受体的配体结合特性和酪氨酸激酶活性，以及人胰岛素受体的2种亚型（HIR-A和-B）的表达。来自正常和肾细胞癌组织的部分纯化的胰岛素和IGF-I受体对其配体具有相同的亲和力。然而，肾细胞癌含有比邻近正常肾组织多3至4倍的特异性胰岛素结合位点和2倍的IGF-I结合位点。此外，我们还测定了两种组织中胰岛素/IGF-I受体杂合体的相对含量。肾细胞癌和邻近的正常组织显示出相似量的胰岛素/IGF-1受体杂合体，即，正常组织中示踪剂IGF-I结合率为44 ± 8.2%，肾细胞癌中为46 ± 12.0%。当研究等量的胰岛素和IGF-I受体蛋白时，我们发现癌组织中受体自磷酸化显着增加，底物磷酸化升高。为了评估胰岛素受体酪氨酸激酶活性的差异是否由胰岛素受体亚型表达模式的改变引起，我们测定了HIR-A和-B的mRNA水平。然而，2种胰岛素受体亚型在正常组织和肿瘤组织中的表达比例差异很大。我们的实验表明，肾癌表达胰岛素和IGF-I受体蛋白的量增加，各自具有增加的特异性自磷酸化和酪氨酸激酶活性。肾癌中胰岛素受体酪氨酸激酶活性的增加不能用胰岛素受体亚型表达模式的改变来解释。© 1995 Wiley利斯公司
We studied expression and functional characteristics of the insulin‐ and insulin‐like‐growth‐factor‐1(IGF‐1) receptors in human renal carcinoma. Ligand‐binding properties and tyrosine‐kinase activity of both receptors, as well as the expression of the 2 isoforms of the human insulin receptor (HIR‐A and ‐B) were analyzed in renal carcinoma and normal adjacent kidney tissue of 8 adult patients. Partially purified insulin‐ and IGF‐I receptors from normal and renal cell carcinoma tissue possessed identical affinities for their ligands. Renal cell carcinoma, however, contained 3‐ to 4‐fold more specific insulin‐binding sites and 2‐fold more IGF‐I binding sites than adjacent normal kidney tissue. In addition, we determined the relative content of insulin/IGF‐I receptor hybrids in both tissues. Renal cell carcinoma and adjacent normal tissue revealed similar amounts of insulin/IGF‐l receptor hybrids, i.e., 44 ± 8.2% of tracer IGF‐I binding in normal tissue and 46 ± 12.0% in renal cell carcinoma. When equal amounts of insulin‐ and IGF‐I receptor protein were studied, we found significantly increased receptor autophos‐ phorylation and elevated substrate phosphorylation in carcinoma tissue. To assess whether the differences in insulin‐receptor tyrosine‐kinase activity were caused by an altered pattern of insulin receptor isoform expression, we determined mRNA levels for HIR‐A and ‐B. The 2 insulin receptor isoforms were, however, expressed in highly variable ratios in both normal and tumor tissue. Our experiments show that renal carcinoma expresses an elevated amount of insulin‐ and IGF‐I receptor protein with increased specific autophosphorylation and tyrosine‐kinase activity each. The increase of insulin‐receptor tyrosine‐kinase activity in renal carcinoma cannot be explained by an altered expression pattern of insulin receptor isoforms. © 1995 Wiley‐Liss, Inc.
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10.1016/0006-291x(80)91591-0
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影响因子：
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