Yoshimura M, Nishikawa M, Mori Y, Yoshikawa N, Horimoto M, Toyoda N, Inada M
Second Department of Internal Medicine, Kansai Medical University, Osaka, Japan.
Thyroid. 1992 Winter;2(4):315-9. doi: 10.1089/thy.1992.2.315.
To elucidate the gene regulation of the thyroid-cell growth-promoting activity by human chorionic gonadotropin (hCG), we investigated the effect of hCG on c-myc proto-oncogene expression in cultured rat FRTL-5 cells by the Northern blot method. hCG induced c-myc mRNA expression, which peaked at 60-120 min. A dose-dependent increase in c-myc mRNA levels was also ascertained. In the presence of crude immunoglobulin G (IgG) from 2 patients with primary hypothyroidism who had blocking type TSH-receptor antibody, c-myc mRNA expressions induced by hCG were decreased to 82% and 62%, compared with that in the presence of normal IgG. The present results suggest that the expression of c-myc mRNA is a part of the molecular mechanism through which hCG regulates the proliferation of thyroid cells, and that hCG-induced c-myc mRNA expression is presumed to be mediated in part by TSH receptors.
为阐明人绒毛膜促性腺激素(hCG)对甲状腺细胞生长促进活性的基因调控作用,我们采用Northern印迹法研究了hCG对培养的大鼠FRTL-5细胞中c-myc原癌基因表达的影响。hCG诱导c-myc mRNA表达,在60 - 120分钟时达到峰值。还确定了c-myc mRNA水平呈剂量依赖性增加。在来自2例患有阻断型促甲状腺激素(TSH)受体抗体的原发性甲状腺功能减退症患者的粗制免疫球蛋白G(IgG)存在的情况下,与正常IgG存在时相比,hCG诱导的c-myc mRNA表达分别降低至82%和62%。目前的结果表明,c-myc mRNA的表达是hCG调节甲状腺细胞增殖的分子机制的一部分,并且推测hCG诱导的c-myc mRNA表达部分是由TSH受体介导的。