我们前期研究中发现Cortactin 与肠癌的侵袭转移密切相关，而肠癌细胞的休眠／增殖是其复发和转移的主要根源，为研究Cortactin 及相关肌动蛋白装配与其关系及调节机制，我们构建了三维细胞培养体系同时结合动物模型实验观察肠癌细胞的休眠和增殖时期，检测不同时期的癌细胞 Cortactin的表达及其边缘肌动蛋白的变化情况，构建病毒载体调节Cortactin的表达，观察癌细胞休眠产生和解除的时间变化以及细胞边缘肌动蛋白形态变化、中心体复制及染色质的异常，分析其周期的改变及细胞有丝分裂相关的中心体功能和 纺锤体定位的不同，构建 Cortactin-src的FRET 生物传感器，活体细胞检测src 对Cortactin 的磷酸化位点的调节导致细胞周期的变化，研究结合 Cortactin 及其介导的肌动蛋白装配与大肠癌的有丝分裂调控信号路径将揭示一种大肠癌休眠发生、休眠与增殖转换的可能的新机制。

Our early studies demonstrated that Cortactin promote invasion and metastasis of colorectal cancer. Colorectal cancer cells dormant / proliferation is a major .source of recurrence and metastasis, for study the relationship between Cortactin and actin protein assembly and colorectal cancer cells dormant / proliferation .and its regulation mechanism, we constructed three-dimensional cell culture system and animal model experiments to observe the period of dormant and .proliferation of cancer cells, to detect cancer cells of the expression of Cortactin and the actin changes on the edge of cell in different periods .Construct viral .vector adjustment Cortactin expression and observe time change in cancer cell dormancy and remove and the cell edge actin morphology changes and .centrosome replication and chromatin abnormalities, analysis of its change of cycle and cell mitotic centrosome function and spindle positioning different, .construct Cortactin-src of the FRET biological sensors, detect the changes of the cell cycle in vivo cell by src regulating the phosphorylation of Cortactin, study .may reveal a new mechanism of colorectal cancer dormancy and proliferation conversion by combine Cortactin and its actin polymerization assembly with mitotic .regulation of signal path of colorectal cancer.