Analysis of the effects of cell growth and cell death regulation on tumor development using tumor mice models

组成活性Ras在肝脏中特异性表达的转基因小鼠（rasv12 -肝小鼠）发生肝细胞癌（HCC）。我们发现ras转基因小鼠在缺乏Tob蛋白的情况下更容易发生HCC。此外，Tob蛋白缺失时，肿瘤的大小明显增大。这些数据表明Tob是抑制HCC发展和增殖的原因。我们还检测了缺乏Tob的rasv12 -肝小鼠和rasv12 -肝小鼠之间基因表达的差异。我们观察到参与细胞生长和死亡调控的几个基因的表达变化。在10多个小鼠样本中同样检测到这些基因的表达变化，表明这些基因对HCC的发展至关重要。

Transgenic mice in which constitutively active Ras is specifically expressing in the liver (RasV12-liver mice) develop hepatocellular carcinoma (HCC). We found that the Ras-transgenic mice much more frequently develop HCC in the absence of Tob protein. Furthermore, the size of the tumors was obviously larger in the absence of Tob protein. These data suggest that Tob is responsible for suppressing HCC development and proliferation. We also examined the difference of gene expression between RasV12-liver mice and RasV12-liver mice lacking Tob. We observed the expression change in several genes involved in cell growth and death regulation. The expression change of those genes was similarly detected in more than ten mice samples, indicating that those genes are critically responsible for HCC development.