中文摘要：

目的 前期研究发现,组蛋白去乙酰化酶抑制剂（HDACi） Scriptaid、TSA分别联合芬维A胺能诱导人肝癌细胞凋亡,RARβ和Nur77可能在其中起重要作用.本研究将探讨RARβ和Nur77在芬维A胺及HDACi对肝癌作用中的相互调控.方法 利用RNA干扰技术人为敲低肝癌细胞Huh-7 RARβ或Nur77基因表达,用芬维A胺（10μM）、组蛋白去乙酰化酶抑制剂Scriptaid（10μM）、TSA（1μM）处理后,利用实时荧光定量PCR检测Nur77 mRNA及RARβ mRNA表达水平.结果 人为敲低RARβ基因表达,对HDACi及芬维A胺处理Huh-7细胞后Nur77 mRNA表达无显著影响（P＞0.05）,同样,人为敲低Nur77基因表达,对HDACi及芬维A胺处理Huh-7细胞后RARβ mRNA表达亦无影响（P＞0.05）.结论 在HDACi及芬维A胺对肝癌细胞作用中,未发现RARβ和Nur77之间存在基因转录水平的相互调控.

英文摘要：

Objective We have previously shown that histone deacetylase inhibitors （HDACi） Scriptaid, TSA and Fenretinide induced apoptosis of Huh-7 cells. Besides, RARfl and Nur77 might play important roles. In this study, we explored interaction between RARfl and Nur77 in Fenretinide or HDACi-induced anticancer effect in hepatocellular carcinoma （HCC） cells. Methods Huh-7 cells were transfected with scramble siRNA, RARfl siRNA and Nur77 siRNA respectively, followed by Fenretinide （10 ~M） or Scriptaid （10/zM） or TSA（1 p~M） treatment. RARfl and Nur77 mRNA levels were measured by real-time RT-PCR. Results RARfl siRNA transfection successfully reduced RAR/3 mRNA expression, but did not affect Fenretinide or HDACi-induced Nur77 mRNA expression. Likewise, knockdown in the expression of Nur77 was not accompanied with reduction of RARfl mRNA level in fenretinide or HDACi treatment. Conclusions There is no interaction between RARfl and Nut77 in mRNA level in Fenretinide or HDACi-induced anticancer effect in hepatocellular carcinoma.