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目的 许多生长因子如表皮生长因子 (EGF) ,与肿瘤的发生密切相关。EGF与表皮生长因子受体 (EGFR)结合 ,通过一系列的信息传导 ,导致肝癌细胞的增生。但受体后的信息传导机制尚不清楚。本实验探讨酪氨酸激酶、蛋白激酶C、Na+/H+交换、钙调蛋白和电压依赖性钙通道在EGF促肝癌细胞生长中的作用。方法 本研究于无血清RPMI164 0中培养肝癌细胞SMMC772 1,采用3 H Thymidine(3 H TdR)掺入的方法 ,检测肝癌细胞DNA合成速率 ,研究酪氨酸激酶、蛋白激酶C、Na+/H+交换、钙调蛋白和电压依赖性钙通道在EGF促肝癌细脆生长中的作用。结果 EGF 10 -9M对肝癌细脆的生长有极显著促进作用 ,与对照组比较差异有显著意义 (P <0 0 5 ) ,酪氮酸激酶阻滞剂Genistein对EGF的促肝癌细胞生长作用具有极显著抑制作用 (P <0 0 0 1)。钙调蛋白阻滞剂W 7、蛋白激酶C阻滞剂H 7和Na+/H+交换阻滞剂amiloride对EGF的促肝癌细胞生长作用具有显著抑制作用 (P <0 0 0 1,P <0 0 1,P <0 0 5 ) ,而对基础状态细胞的3 H TdR掺入值无显著影响 (P >0 0 5 )。电压依赖性钙通道阻滞剂Varapamil对BGF的促肝癌细胞生长作用无显著抑制作用 (P >0 0 5 ) ,对基础状态细胞的3 H TdR掺入值亦无显著影响 (P >0 0 5 )。结论 结果显示 ,酪氨酸激酶、?
Purpose Many growth factors such as epidermal growth factor (EGF) are closely related to tumorigenesis. EGF and epidermal growth factor receptor (EGFR) binding, through a series of information transmission, resulting in the proliferation of liver cancer cells. However, the mechanism of post-receptor information transmission is not clear. This study explored the role of tyrosine kinase, protein kinase C, Na + / H + exchange, calmodulin and voltage-dependent calcium channels in the growth of hepatocellular carcinoma cells. Methods In this study, hepatoma SMMC772 cells were cultured in serum-free RPMI1640 medium. The DNA synthesis rate of hepatocellular carcinoma cells was detected by 3 H Thymidine incorporation assay. The effects of tyrosine kinase, protein kinase C, Na + / H + exchange , Calmodulin and voltage-dependent calcium channels in promoting the growth of small and delicate hepatocarcinoma cells. Results EGF 10 -9M could significantly promote the growth of small and delicate hepatocellular carcinoma cells, which was significantly different from that of the control group (P <0.05). Genistein, a tyrosine kinase inhibitor, had an inhibitory effect on the growth of hepatocarcinoma cells Very significant inhibition (P <0 0 0 1). Calmodulin blocker W7, protein kinase C inhibitor H7 and Na + / H + exchange blocker amiloride significantly inhibited the growth of hepatocarcinoma cells induced by EGF (P <0.01 1, P <0 0 1, P <0 05), but had no significant effect on the incorporation of 3 H TdR in basal cells (P> 0.05). Varapamil, a voltage-dependent calcium channel blocker, showed no significant inhibitory effect on BGF-induced hepatocarcinoma cell growth (P> 0.05), but also had no significant effect on the incorporation of 3 H TdR in basal cells (P> 0.05) ). Conclusion The results show that tyrosine kinase,?