子宫内膜癌（EC）发病率逐年升高且呈年轻化趋势，其靶向药物是近年来的研究焦点。临床资料显示90%以上的EC有PI3K/Akt/mTOR通路的激活，前期工作证实Hippo通路效应分子YAP1可以上调GAB2激活PI3K/Akt/mTOR通路，与EC的恶性程度及生存时间密切相关。 因此，YAP1可成为EC治疗的新靶点。Verteporfin（VP）是YAP的抑制剂，前期通过细胞实验和动物模型均证实VP具有明显抑制内膜癌细胞增殖和侵袭的作用，降调YAP1导致VP作用减弱。VP如何调节YAP1？目前尚不明了。前期发现VP诱导YAP1的SUMO化，我们推测VP诱导YAP1的SUMO化抑制YAP1的功能，从而发挥抑制EC的作用。本研究将在前期工作基础上，从体内外、多环节验证假设，揭示VP对YAP1的作用机制及其对YAP1功能的影响，为今后针对YAP1为靶点，将VP用于EC靶向治疗提供前期基础。

The incidence of Endometrial cancer (EC) is increasing and the age of population of EC is getting younger. To explore the new targeting drugs is the focus of current oncological studies. The clinic data show more than 90% EC has the activation of PI3K/Akt/mTOR pathway and YAP1 that is the major downstream effector of Hippo pathway could up-regulate GAB2 to active the PI3K/Akt/mTOR pathway and is closed to the malignancy and survival of EC. Therefore, YAP1 could be able to be a promising target for EC target therapy. Verteporfin was revealed as an inhibitor of YAP and we found it has an inhibited effect on proliferation and invasion of EC cells by experiments at the cellular level and animal model. in additional, the effects of VP was relieved by the decrease of YAP1. How does Verteporfin inhibit the function of YAP1, which is unknown in EC. Our previous work preliminarily found the SUMOylation of YAP1 induced by Verteporfin. We hypothesize that Verteporfin could inhibit EC by inducing the SUMOylation of YAP1, which can inhibit the function of YAP1. Based on our previous work, this study will validate our hypothesis deeply via in vivo and in vitro and explore the mechanism of SUMOylation of YAP1 by Verteporfin as well as the effects of SUMOylation of YAP1 on EC cells. It will provide the evidences that support the therapy targeting YAP1 for EC and the possibility that Verteporfin could be able to be a new promising drug for the targeting therapy of EC in the future.