Prince Henry's Institute of Medical Research, PO Box 5152, Clayton, Victoria 3168, Australia.
Mol Cell Endocrinol. 2012 Aug 15;359(1-2):85-91. doi: 10.1016/j.mce.2011.07.033. Epub 2011 Aug 4.
Ovarian cancer may be the most frequently lethal gynaecological malignancy but the heterogeneous nature of the disease and the advanced stage at which it is usually diagnosed, have contributed to the paucity of information relating to its aetiology and pathogenesis. Members of the TGF-β superfamily, estrogen and NFκB have all been implicated in the development and progression of cancers from a wide range of tissues. In the ovary, TGF-β superfamily members and estrogen play key roles in maintaining normal function. To date, little is known about the capacity of NFκB to influence normal ovarian function except that it is ubiquitously expressed. In this review we will highlight the roles that inhibin/activin, estrogen and NFκB, have been attributed within carcinogenesis and examine the potential for crosstalk between these pathways in ovarian cancer pathogenesis.
卵巢癌可能是最常见的致命妇科恶性肿瘤，但由于该病的异质性以及通常在晚期诊断，因此与发病机制相关的信息很少。TGF-β 超家族、雌激素和 NFκB 的成员都与多种组织来源的癌症的发生和发展有关。在卵巢中，TGF-β 超家族成员和雌激素在维持正常功能方面发挥着关键作用。迄今为止，除了 NFκB 普遍表达外，人们对其影响正常卵巢功能的能力知之甚少。在这篇综述中，我们将重点介绍抑制素/激活素、雌激素和 NFκB 在癌变过程中所扮演的角色，并研究这些途径在卵巢癌发病机制中的相互作用的潜力。
