肝癌小鼠模型 z-bo 2020-12-21 282

　　Recently, researchers from Baylor College of Medicine in the United States published a new study in the international journal Nature Communication. They found that the co-activation of nuclear exogenous receptor CAR and β catenin can induce the proliferation of differentiated liver cells in mice, leading to cell proliferation. Out of control, liver cancer occurs. The results of this research prove that the mouse model of liver cancer is directly related to human HCC. Therefore, it is of greater significance to use the mouse model of liver cancer for drug development and basic research.

　　 The researchers mentioned in the article that the abnormal expression of β catenin can promote the occurrence of human liver cancer, but the activation of β catenin alone is not enough to induce the occurrence of liver cancer in mice. They found that the acute activation of β catenin and nuclear exogenous receptor CAR can induce the proliferation of differentiated liver cells. Under normal circumstances, these responses are strictly limited and closely related. In CAR-dependent tumors induced by phenobarbital In almost all cases, β catenin activation occurred. Researchers have confirmed that full activation of β catenin in the liver can induce cell senescence and growth arrest. When CAR is activated at the same time, although the liver still has normal functions, cell senescence and growth arrest disappear, and uncontrolled cell proliferation and hepatomegaly appear. And rapid lethality. CAR activation and partial activation of β catenin can induce tumorigenesis, and these tumor cells have similar conservative gene expression to β catenin-positive human HCC. "To sum up, the results of this article show that the co-activation of CAR and β catenin can induce hepatocarcinogenesis, and at the same time defines the direct relationship between the mouse model of liver cancer and human HCC.