Goretzki P E, Koob R, Koller C, Röher H D
Acta Endocrinol Suppl (Copenh). 1987;281:273-80. doi: 10.1530/acta.0.114s273.
Monolayer cultures of human thyrocytes from normal thyroids (n = 13), thyroid adenomas (n = 8), differentiated (n = 7), poorly and undifferentiated (n = 5) thyroid cancers as well as thyroid cancer metastases (n = 2) were established to assess the significance of TSH and cAMP on cell growth and DNA synthesis. Cell growth was stimulated by 0.1 IU bTSH/ml and inhibited by 1.0 IU bTSH/ml (P less than 0.01), while dibutyryl-cAMP (dbcAMP) failed to show any effect on cell growth at the concentrations (10-5; 10-3 mol/l), tested. Neither did the adenylate-cyclase inhibitor dideoxy-adenosine (ddA) (2 X 10-5 mol/l) stimulate thyrocyte growth. DNA synthesis, however, measured indirectly by [3H]thymidine incorporation, was stimulated not only by TSH 2-12-fold, but also by ddA 1.3-7-fold (P less than 0.01), and was not affected by dbcAMP. TSH had no effect on [3H]thymidine incorporation in fibroblasts and c-cells from c-cell carcinomas. The stimulatory effect of TSH on thyrocyte growth and DNA synthesis was unpredictable in thyrocytes from cancerous tissues (n = 14) with no obvious correlation to tumour differentiation or stage. Thus, we showed that TSH is a promotor for cell growth and DNA synthesis in monolayer cultures of human thyrocytes from normal and adenomatous human thyroid tissues with no obvious correlation to the AC system. This TSH effect is unpredictable, however, in thyrocytes from human thyroid cancer.
建立了来自正常甲状腺（n = 13）、甲状腺腺瘤（n = 8）、分化型（n = 7）、低分化和未分化型（n = 5）甲状腺癌以及甲状腺癌转移灶（n = 2）的人甲状腺细胞单层培养物，以评估促甲状腺激素（TSH）和环磷酸腺苷（cAMP）对细胞生长和DNA合成的意义。0.1 IU bTSH/ml刺激细胞生长，1.0 IU bTSH/ml抑制细胞生长（P < 0.01），而在测试浓度（10⁻⁵；10⁻³ mol/l）下，二丁酰环磷腺苷（dbcAMP）对细胞生长无任何影响。腺苷酸环化酶抑制剂双脱氧腺苷（ddA）（2×10⁻⁵ mol/l）也不刺激甲状腺细胞生长。然而，通过[³H]胸腺嘧啶核苷掺入间接测量的DNA合成，不仅受到TSH 2 - 12倍的刺激，也受到ddA 1.3 - 7倍的刺激（P < 0.01），且不受dbcAMP影响。TSH对成纤维细胞和来自C细胞癌的C细胞中的[³H]胸腺嘧啶核苷掺入无影响。TSH对癌组织（n = 14）的甲状腺细胞生长和DNA合成的刺激作用不可预测，与肿瘤分化或分期无明显相关性。因此，我们表明TSH是正常和腺瘤性人甲状腺组织的人甲状腺细胞单层培养中细胞生长和DNA合成的促进剂，与腺苷酸环化酶（AC）系统无明显相关性。然而，这种TSH效应在人甲状腺癌的甲状腺细胞中是不可预测的。
