Kon O L
Bioessays. 1989 Jun;10(6):210-4. doi: 10.1002/bies.950100608.
The classical estrogen receptor model does not sufficiently account for the tumor-promoting activity of estrogens or for the antiproliferative effect of anti-estrogens in estrogen-dependent tumors. Particular difficulties not readily accommodated within the model are that hormonal autonomy can supervene without loss of the estrogen receptor and that antiestrogen effects are highly context-dependent, without apparent differences in the estrogen receptor itself or in metabolic transformation of antiestrogens. Recent studies suggest that estrogens may promote cell proliferation, in part, through the mediation of growth factors and that antiestrogens may exert some of their effects by mechanisms unrelated to the estrogen receptor.
经典的雌激素受体模型不足以解释雌激素的促肿瘤活性或抗雌激素在雌激素依赖性肿瘤中的抗增殖作用。该模型难以轻易解释的特殊困难在于,激素自主性可以在不丧失雌激素受体的情况下出现,而且抗雌激素的作用高度依赖于环境,在雌激素受体本身或抗雌激素的代谢转化方面没有明显差异。最近的研究表明,雌激素可能部分通过生长因子的介导促进细胞增殖,而抗雌激素可能通过与雌激素受体无关的机制发挥其部分作用。