子宫内膜癌转移与预后相关，转移机制不清。肿瘤转移灶与原发灶间存在基因异质性。目前癌基因介导骨架重构与能量代谢重编程成为肿瘤转移研究热点。本课题组前期对不同转移能力内膜癌细胞进行cofilin通路介导骨架重构进行研究；同时对内膜癌转移组织基因筛查发现转移相关新融合基因DPH7-PTP4A3。文献显示PTP4A3可调控cofilin通路，引起细胞骨架F-actin重构，介导肿瘤转移；DPH7可能调控NF-κB通路，参与癌转移细胞能量代谢。据此提出假说：子宫内膜癌转移相关融合基因通过“cofilin/PGC-1α双信号通路，调控骨架与代谢双功能介导内膜癌转移”学说。本课题拟通过上调/下调DPH7、PTP4A3和DPH7-PTP4A3，在体内外验证融合基因对子宫内膜癌转移的作用，并研究DPH7和PTP4A3的调控机制，为子宫内膜癌转移研究提供新思路，为靶向治疗提供新靶点。

Advanced endometrial cancer is prone to metastasis and has a poor prognosis. There were different fusion genes between primary and metastasis tumour tissue. Nowadays, the study of cytoskeleton reconstruction and energy metabolism reprogramming mediated by genes has become the hotspot in tumor metastasis. Our studies have showed that the invasion ability of endometrail cancer cells was affected by cofilin pathway. Meanwhile, DPH7-PTP4A3, a new fusion gene, were identified in endometrial cancer and proved to play vital role in endometrial cancer metastasis. In the literature, it has been shown that PTP4A3 gene may cause cytoskeleton reconstruction by activating cofilin pathway. DPH7 gene could regulate energy metabolism reprogramming by activating NF-κB pathway. Therefore, we proposed the hypothesis that new fusion gene DPH7-PTP4A3 may regulate cytoskeleton reconstruction through cofilin pathway and energy metabolism through PGC-1αpathway, which may bring ablout endometrial cancer metastasis. To verify the hypothesis, new fusion gene DPH7-PTP4A3 was been knocked-down and over-expressed, to study the metastasis mechanism of endometrial cancer cells in vivo and in vitro, which provide an ideal method for the study of endometrial cancer metastasis.