Chou C K, Su T S, Chang C M, Hu C P, Huang M Y, Suen C S, Chou N W, Ting L P
Department of Medical Research, Veterans General Hospital, Taipei, Taiwan, Republic of China.
J Biol Chem. 1989 Sep 15;264(26):15304-8.
The human hepatoma Hep3B cells contain integrated hepatitis B viral genome and continually secret hepatitis B surface antigen (HBsAg). The production of HBsAg (but not alpha-fetoprotein) was suppressed by addition of low concentrations (0.1-1 nM) of insulin into serum-free medium. In addition, the suppression of HBsAg production by insulin was paralleled with the decrease in HBsAg mRNA abundance. Insulin also cause a rapid rate of disappearance of HBsAg mRNA (t 1/2, 2 h) in Hep3B cells. The Hep3B cells carry specific receptor with high affinity for insulin (Kd = 1.8 nM). The receptor showed an insulin-dependent protein tyrosine kinase activity. The half-maximal insulin concentration for the activation of the receptor kinase was about 5 nM. Only very high concentrations of insulin-like growth factor I and human proinsulin can compete for the insulin receptor binding and suppress HBsAg production, this suggests that insulin may act through its receptor binding to suppress HBsAg expression in human hepatoma Hep3B cells.
人肝癌Hep3B细胞含有整合的乙型肝炎病毒基因组，并持续分泌乙型肝炎表面抗原（HBsAg）。在无血清培养基中添加低浓度（0.1 - 1 nM）的胰岛素可抑制HBsAg（而非甲胎蛋白）的产生。此外，胰岛素对HBsAg产生的抑制作用与HBsAg mRNA丰度的降低相平行。胰岛素还导致Hep3B细胞中HBsAg mRNA快速消失（半衰期为2小时）。Hep3B细胞携带对胰岛素具有高亲和力的特异性受体（解离常数Kd = 1.8 nM）。该受体显示出胰岛素依赖性蛋白酪氨酸激酶活性。激活受体激酶的半数最大胰岛素浓度约为5 nM。只有非常高浓度的胰岛素样生长因子I和人胰岛素原能够竞争胰岛素受体结合并抑制HBsAg产生，这表明胰岛素可能通过其受体结合来抑制人肝癌Hep3B细胞中HBsAg的表达。
