Study on abnormality in growth regulation hepatic carcinogenesis and its control.

我们研究了人类肝癌发生的分子机制，从肝细胞由于对一种强效负生长调节剂tgf - β的反应性丧失而具有自主增殖潜力的观点出发。先前，我们发现人肝癌来源的细胞系对tgf - β的反应较差。肝细胞癌（HCC）发生在hbv或hcv相关肝硬化的肝脏中。我们将HBx基因导入对tgf - β非常敏感的水貂肺上皮细胞。转染细胞对tgf - β的反应性远不如亲本细胞。此外，反应性降低似乎是由于tgf - β受体表达减少所致。慢性HBV感染过程中，肝细胞可通过HBx基因的表达摆脱tgf - β的负生长调控。

We have studied molecular mechanisms of human hepatocarcinogenesis from the view of the point that hepatocytes have an autonomous proliferative potential due to a loss of the responsiveness to a potent negative growth regulator, TGF-beta. Previously, we found poor response of human hepatoma-derived cell lines to TGF-beta.Hepatocellular carcinoma (HCC) occurs in the liver with HBV-or HCV-related cirrhosis. We introduced HBx gene into mink lung epithelial cell, a cell line which is very sensitive to TGF-beta. The responsiveness to TGF-beta in the transfectants was much poorer than that in the parent cells. In addition, the reduced responsiveness seemed to result from a decrease in expression of TGF-beta receptors. The hepatocytes could escape from the negative growth regulation by TGF-beta due to expression of HBx gene during chronic HBV infection.