Steroid receptor coactivator-3, a homolog of Taiman that controls cell migration in the Drosophila ovary, regulates migration of human ovarian cancer cells
Steroid receptor coactivator-3, a homolog of Taiman that controls cell migration in the Drosophila ovary, regulates migration of human ovarian cancer cells
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DOI：
10.1016/j.mce.2005.10.008
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发表时间：
2005-12-21
影响因子：
4.1
通讯作者：
Naora, H
中科院分区：
文献类型：
--
作者：
Yoshida, H;Liu, JS;Naora, H
边界细胞迁移是果蝇卵巢发育过程中发生的一个过程，其中源自简单上皮的细胞迁移并侵入邻近组织。这个过程类似于源自人类卵巢简单上皮的癌细胞的行为。边界细胞迁移的一个重要调节因子是 Taiman，它是类固醇受体辅激活因子 3 (SRC-3) 的同源物。由于越来越多的证据表明边界细胞和癌细胞迁移的分子控制之间存在相似性，因此我们研究了 SRC-3 是否控制卵巢癌细胞迁移。在正常卵巢表面上皮、卵巢囊肿和缺乏间质侵袭的交界性卵巢肿瘤中检测到很少或没有检测到SRC-3表达。相反，SRC-3在高级别卵巢癌中大量表达。抑制卵巢癌细胞中的 SRC-3 表达可显着减少细胞扩散和迁移，并改变粘着斑激酶的细胞内定位。这种对细胞迁移的抑制作用与细胞的雌激素受体（ER）状态无关。这些研究揭示了 SRC-3 通过促进细胞迁移在卵巢癌进展中的新作用，独立于其在雌激素受体信号传导中的作用。 (c) 2005 Elsevier Ireland Ltd. 保留所有权利。
Border cell migration is a process that occurs during Drosophila ovarian development in which cells derived from a simple epithelium migrate and invade neighboring tissue. This process resembles the behavior of cancerous cells that derive from the simple epithelium of the human ovary. One important regulator of border cell migration is Taiman, a homolog of steroid receptor coactivator-3 (SRC-3). Because increasing evidence indicates that similarities exist between the molecular control of migration of border cells and of cancer cells, we investigated whether SRC-3 controls ovarian cancer cell migration. Little or no SRC-3 expression was detected in normal ovarian surface epithelium, ovarian cysts and borderline ovarian tumors that lack stromal invasion. In contrast, SRC-3 was abundantly expressed in high-grade ovarian carcinomas. Inhibiting SRC-3 expression in ovarian cancer cells markedly reduced cell spreading and migration, and altered intracellular localization of focal adhesion kinase. This inhibitory effect on cell migration was independent of the estrogen receptor (ER) status of the cells. These Studies reveal a novel role for SRC-3 in ovarian cancer progression by promoting cell migration, independently of its role in estrogen receptor signaling. (c) 2005 Elsevier Ireland Ltd. All rights reserved.