血管生成拟态（VM）已被证实是除血管外为肿瘤提供血液的新途径，抑制其形成有望提高肿瘤治疗效果。研究显示环氧合酶2（COX-2）与大肠癌发生进展关系密切，可激活下游信号通路诱导肠癌VM形成。另据报道VE-Cadherin信号通路是调控肠癌VM形成的关键途径，受诸多上游信号调控。二者间是否存在调控关联目前尚不明确。.申请人前期临床研究发现以健脾祛湿，祛瘀解毒为治法的抑癌方能够改善肠癌预后，进一步实验发现该方可以抑制结肠癌VM形成，并能影响COX-2、VE-Cadherin蛋白表达。故推测抑癌方可能通过干预COX-2调控VE-Cadherin信号通路抑制结肠癌VM形成。为证实假说，本课题拟在前期基础上进一步明确：（1）COX-2和VE-Cadherin信号通路之间是否存在调控关系及在肠癌VM形成中的作用；（2）抑癌方对COX-2和VE-Cadherin信号通路的影响。藉此探究抑癌方的作用机制。

Vasculogenic mimicry (VM) has been proved to be a new way of tumor blood supply besides the blood vessels. To inhibit tumor VM formation is expected to increase the therapeutic effect. Studies have shown that COX-2 is closely related with the occurrence and development of colorectal cancer, which can also induce the formation of VM by activating downstream signaling pathways. According to another reports, VE-Cadherin signaling pathway is a key way of regulating the VM formation of colon cancer regulated by many upstream signals. But whether there is correlation between this two is unclear so far..Our previous experiments have found Yiai decoction (YAD) can inhibit the colon cancer and the VM formation in which, and the expression of COX-2, VE-Cadherin. Accordingly, we infer YAD may intervene VE-Cadherin signaling pathway regulated by COX-2 to inhibit colon cancer VM formation. To confirm this hypothesis, this study intends to further clarify on the basis of the preliminary: (1) Whether there is relation between COX-2 and VE-Cadherin signaling pathway and their roles in colon cancer VM formation; (2) the effect of YAD on COX-2 and VE-Cadherin signaling pathway. Our aim is to explore the mechanism of effect of YAD.