Selzer E, Schiferer A, Hermann M, Grubeck-Loebenstein B, Freissmuth M
Institute of Pharmacology, Vienna.
Thyroidology. 1992 Apr;4(1):7-10.
The molecular mechanisms underlying the development of endocrine active thyroid tumors are poorly understood. These tumors produce excess thyroid hormone, which then suppresses TSH (thyroid stimulating hormone) production. In the present report, we show that the expression of Gi alpha-1 is under control of TSH in the normal human thyroid. In contrast Gi alpha-1 escapes TSH control in autonomous adenoma and thus is constitutively expressed. Since receptor-mediated activation of Gi controlled pathways is known to elicit a proliferative response in several cell types, we propose that in thyroid adenomas the unregulated constitutive expression of Gi alpha-1 is causally related to the autonomous growth.
内分泌活性甲状腺肿瘤发生的分子机制目前仍知之甚少。这些肿瘤会产生过量的甲状腺激素，进而抑制促甲状腺激素（TSH）的分泌。在本报告中，我们发现正常人甲状腺中Giα-1的表达受TSH调控。相反，在自主性腺瘤中，Giα-1不受TSH控制，因此持续表达。由于已知Gi控制的途径经受体介导激活会在几种细胞类型中引发增殖反应，我们推测在甲状腺腺瘤中，Giα-1不受调控的持续表达与自主性生长存在因果关系。
