卵巢癌的死亡率高居妇科肿瘤之首。其中，肿瘤细胞的高转移率是其预后不良的一个重要原因。深入研究卵巢癌细胞转移的分子机制，对于发现新的肿瘤标志、药物靶点、发展新的抗卵巢癌治疗策略具有重要价值。最近，我们应用组织芯片发现，Ikaros，一种造血系统转录调节因子，在多种卵巢癌组织中高表达，并与浆液性卵巢腺癌的恶性程度和转移正相关，但在正常卵巢组织中不表达或弱表达。进一步，我们发现，Ikaros可通过上调上皮-间质转化因子Slug和MMP2，下调E-cadherin和β-catenin等促进卵巢癌细胞的迁移和侵袭。本项目拟在此基础上，深入研究Ikaros上调Slug表达的分子机制；探索Ikaros在卵巢癌中过表达的分子机制；并通过制备在卵巢特异表达Ikaros的转基因小鼠明确Ikaros与卵巢癌发生和发展的可能关系。这些研究有望揭示新的卵巢癌转移机制，从而为卵巢癌的抗转移治疗提供新的策略。

Ovarian cancer is one of the most common gynecological malignancy and the leading causes of death from gynecological cancers in women. Understanding the metastatic mechanism is crucial for developing novel treatment strategy for ovarian cancer. Recently, we found that the Ikaros, a key regulator of lymphocyte differentiation, expressed higher in ovarian cancer tissues compared with normal ovarian tissues and significantly associated with the high FIGO Stage and low differentiation state in ovarian serous adenocarcinoma carcinoma. Moreover, we demonstrated that overexpression of Ikaros in ovarian cancer cell lines increased cell migration and invasion by up-regulation of Slug but not Snail1, with a concomitant decrease of E-cadherin and increase of MMP-2. Furthermore, knockdown of Slug inhibited Ikaros-induced cell migration and invasion. These findings presenting a new insight for the metastasis of ovarian cancer cells and further studies on Ikaros-induced Slug up-regulation may provide novel target for inhibiting ovarian cancer metastasis.