Rotsch M, Maasberg M, Erbil C, Jaques G, Worsch U, Havemann K
Philipps-University Marburg, Department of Internal Medicine, Federal Republic of Germany.
J Cancer Res Clin Oncol. 1992;118(7):502-8. doi: 10.1007/BF01225264.
Small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC) cell lines were studied for insulin-like growth factor I (IGF-I) receptor expression and with regard to the influence of IGF-I on cell proliferation. IGF-I receptors on the cells were characterized by competitive binding assays, chemical crosslinking and northern blot hybridization of IGF-I receptor mRNA. All SCLC and NSCLC cell lines showed specific IGF-I binding sites with an affinity (KD) of 0.69-5.21 nM. The amount of binding sites ranged from 59 fmol/mg to 1230 fmol/mg protein. The IGF-I binding was inhibited by the IGF-I receptor antibody (alpha-IR-3). Northern blot hybridization indicated that IGF-I receptor mRNA was being produced by all SCLC and NSCLC cell lines. We used the soft-agarose clonogenic assay to evaluate the influence of IGF-I on the in vitro proliferation of the cells. Our results have shown that IGF-I stimulates the growth of all tested cell lines ranging from a factor of 1.6 to 4.2 in SCLC and from 1.1 to 2.7 in NSCLC. The data indicate that the IGF-I receptor thus appears to be the common pathway for the mitogenic activity of IGF-I and IGF-II with regard to human lung cancer cells.
对小细胞肺癌(SCLC)和非小细胞肺癌(NSCLC)细胞系进行了胰岛素样生长因子I(IGF-I)受体表达以及IGF-I对细胞增殖影响的研究。通过竞争性结合试验、化学交联和IGF-I受体mRNA的Northern印迹杂交对细胞上的IGF-I受体进行了表征。所有SCLC和NSCLC细胞系均显示出特异性IGF-I结合位点,亲和力(KD)为0.69 - 5.21 nM。结合位点的数量范围为59 fmol/mg至1230 fmol/mg蛋白质。IGF-I结合被IGF-I受体抗体(α-IR-3)抑制。Northern印迹杂交表明所有SCLC和NSCLC细胞系均产生IGF-I受体mRNA。我们使用软琼脂克隆形成试验来评估IGF-I对细胞体外增殖的影响。我们的结果表明,IGF-I刺激所有测试细胞系的生长,在SCLC中刺激因子为1.6至4.2,在NSCLC中为1.1至2.7。数据表明,就人肺癌细胞而言,IGF-I受体似乎是IGF-I和IGF-II促有丝分裂活性的共同途径。