胃癌转移是晚期患者死亡重要原因，CAFs促进胃癌转移进程，血管内皮细胞EndMT转化是CAFs主要来源。我们前期研究发现：胃癌细胞外泌体内lncUCA1诱导血管内皮细胞EndMT转化获得CAFs特性促进胃癌转移。然而，lncUCA1是否通过招募结合ELAV1激活β-catenin/MRTF-A信号通路诱导EndMT尚未有文献报道，相关分子机制尚不明确。为此，我们提出“外泌体lncUCA1激活β-catenin/MRTF-A通路诱导内皮细胞EndMT促进胃癌转移”这一科学假说。为此本项目将重点研究：lncUCA1招募结合ELAV1促进β-catenin激活分子机制；lncUCA1激活β-catenin引起MRTF-A表达导致EndMT分子机制。针对上述问题的研究，将为胃癌转移复发的防治提供新思路、新策略。

Metastasis is strongly responsible for the high death rate of advanced stage gastric cancer (GC) patients. CAFs promotes GC metastasis, which mainly come from endothelial to mesenchyme transition（EndMT）. Our previous study indicated that exosome-lncUCA1 derived from GC could induce EndMT of endothelial cell, which acquire the ability of CAFs to promote GC migration and invasion. However, how exosome-lncUCA1 actives β-catenin/MRTF-A pathway has not been reported, the underlying mechanism was also covered.Therefore，we hypothesize that exosome-lncUCA1 could active β-catenin/MRTF-A pathway to induce EndMT of endothelial cell to promote metastasis of GC. We mainly focus on the analyzing the mechanism of lncUCA1 recruiting ELAV1 to activate β-catenin/ MRTF-A pathway. To investigate and answer these questions may bring new thoughts and new strategy to overcome GC.