肝癌血管生成拟态与肝癌转移侵袭密切相关。研究发现肝癌血管生成拟态的形成与进展受Rho/ROCK信号通路的调控，ROCK在调控中起关键作用；同时肝癌血管生成拟态还涉及肿瘤微环境及癌细胞上皮间质化等因素影响，TGF-β1/CTGF通路与之密切相关；且研究证实Rho/ROCK与TGF-β1/CTGF通路间存在信号串扰。所以我们预测TGF-β1/CTGF通路参与肝癌血管生成拟态调控，而ROCK作为关键信号分子在调控中起核心作用。本研究以不同肝癌细胞株及裸鼠人肝癌模型为研究对象，采用慢病毒、基因沉默、Western等技术检测ROCK、TGF-β1/CTGF及血管生成拟态关键信号分子的转录和表达，研究ROCK在TGF-β1/CTGF通路调控肝癌血管生成拟态的分子机制；阐明鳖甲煎丸对肝癌血管生成拟态的影响及分子机理。本研究将为临床抗肿瘤血管治疗提供新的思路，为鳖甲煎丸的临床应用提供更充分的理论依据。

There is a close relationship between vasculogenic mimicry and migration and invasion in Hepatocellular carcinoma(HCC). It shows that Rho/ROCK signaling pathway, especially ROCK plays a key role in the formation and development of vasculogenic mimicry in HCC. What’s more, tumor micro-environment, epithelial-mesenchymal transition of tumor cells and other factors can also influence vasculogenic mimicry in HCC. It is confirmed that there is signal cross-talk between Rho/ROCK signaling pathway and TGF-β1/CTGF signaling pathway. So we propose that TGF-β1/CTGF signaling pathway regulates vasculogenic mimicry in HCC, in which ROCK plays an core role as a key signal molecule. In this study, hepatoma cell lines with different migration potential and human hepatocellular carcinoma model in nude mice are taken as subjects. Lentivirus, gene silencing, western-blot and other techniques are taken to detect the transpription and expression of key signal molecule in ROCK, TGF-β1/CTGF signaling pathway and vasculogenic mimicry in HCC, so as to declare the molecular mechanism of ROCK, TGF-β1/CTGF signaling pathway in vasculogenic mimicry in HCC and the effect and molecular mechanism of Biejiajianwan on vasculogenic mimicry in HCC. This study will provide not only a new way for the clinic in treating tumor, but also theoretical basis for clinical use of Biejiajianwan.