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

活性RAS在肝脏特异表达的转基因小鼠(RasV12-肝脏小鼠)发生肝细胞癌(HCC)。我们发现，在没有Tob蛋白的情况下，转RAS基因的小鼠更容易发生肝癌。此外，在没有Tob蛋白的情况下，肿瘤的体积明显较大。这些数据表明ToB负责抑制肝细胞癌的发展和增殖。我们还检测了RasV12-肝小鼠和缺失Tob的RasV12-肝小鼠之间的基因表达差异。我们观察了参与细胞生长和死亡调控的几个基因的表达变化。在十多个小鼠样本中也同样检测到了这些基因的表达变化，表明这些基因对肝癌的发展起着至关重要的作用。

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.