血管生成拟态(vasculogenic mimicry, VM)是导致肿瘤侵袭转移的重要机制。研究发现绒癌组织标本中存在VM现象，且构成血管样通道的细胞以合体滋养细胞为主，提示合体滋养细胞与绒癌VM现象密切相关。与滋养细胞合体化密切相关的Forskolin是VM现象的重要诱导因子。目前关于Forskolin通过诱导滋养细胞合体化调控绒毛膜癌VM现象的发生及其分子机制尚且未知。我们的前期研究发现绒毛膜癌细胞株具有血管成形能力，且Notch信号通路与滋养细胞的分化密切相关。因此我们拟以临床滋养细胞肿瘤组织标本及绒癌细胞株为研究对象，观察不同浓度的Forskolin在改变绒癌细胞株合体化程度中对VM现象的影响，同时采用体内外实验观察Notch信号通路调控该现象的分子机制，为临床滋养细胞肿瘤的治疗提供新的思路。

Vascular mimicry (vasculogenic mimicry, VM) is an important mechanism of tumor invasion and metastasis. It has already reported that VM phenomenon was present in choriocarcinoma tissue specimens, and vessel-like passage was mainly constituted by syncytiotrophoblast. Forskolin is not only an inducer of syncytation of trophoblast, but also an inducer of VM in other tumors. Currently, whether the process of forskolin induced trophoblast syncytation is regulating VM in choriocarcinoma and its molecular mechanisms was not yet known. Our previous study showed that choriocarcinoma cell has capability of VM formation, and the Notch signaling pathway is closely related with the differentiation of trophoblast. In this study, we intend to use clinical trophoblastic tumor tissues and choriocarcinoma cell lines to observe the effects of Forskolin on VM phenomenon in vivo and in vitro, when it change the degree of syncytation of trophoblast, and discuss the molecular mechanism of Notch signaling pathway in this phenomenon, to provide new ideas on the treatment of trophoblastic tumors in clinics.