腹腔内播散和远处转移是导致卵巢癌患者死亡的主要因素。上皮-间充质转化（ Epithelial–Mesenchymal Transition， EMT）是卵巢癌转移过程中的关键步骤, 与腹腔转移及与卵巢癌病人的存活率十分相关。本人前期已发表的研究结果证实，Rac1-MEK/Src信号通路可通过EMT过程参与卵巢癌转移，并且MEK1、Src的小分子抑制剂联用能够减少卵巢癌腹腔转移及显著延长动物的存活期。在此基础上，我们发现异甘草素能够抑制MEK1、Src的活性。因此，本项目的是评价异甘草素是否具有逆转卵巢癌 EMT 过程从而抑制卵巢癌转移的作用，并确证其分子机制是否通过Rac1-MEK1/Src信号通路实现的。

High mortality rate of ovarian cancer is most likely to be caused by late diagnosis when patients are already in advanced stages. Almost all of patients will meet their demise owing to metastasis. Like other epithelial-derived tumors, EMT ( Epithelial–Mesenchymal Transition) has been demonstrated as a critical step for ovarian cancer metastasis progression, and is significantly associated with survival of ovarian cancer patients. Our previous study has revealed that Rac1-MEK1/Src signaling pathway is important for ovarian cancer metastasis through sustaining EMT process. Importantly, we demonstrated that combined use of MEK1/2 and Src inhibitors effectively suppresses development of intraperitoneal xenografts and prolongs the survival of ovarian cancer-bearing mice. Based on drug screening, we further found that isoliquiritigenin was able to inhibiting the activation of MEK1 and Src. Thus, this project is aimed to evaluated the anti-metastasis effects of isoliquiritigenin on ovarian cancer, and confirm the critical role of Rac1-MEK1/Src signaling pathway.