中文摘要：

目的研究内质网应激对miR221／222的调控及其在肝癌细胞抵抗内质间应激诱导细胞凋亡中作用。方法采用miR221／222抑制物和miR221／222类似物分别阻断或模拟内源性miR-221／222的功能，并利用Western blot和流式细胞技术分析内质网应激条件下miR-221／222对肝癌细胞周期和凋亡的调控作用。结果内质网应激诱导miR221／222表达下凋，miR221／222类似物和抑制物分别抑制和促进内质网应激诱导的p27Kip1表达上调，干扰p27^kipl不仅抑制了内质网应激诱导的肝癌细胞G0／G1期阻滞，也促进了内质网应激介导的肝癌细胞凋亡。结论内质网应激诱导miR-221／222下调能够通过促进p27^Kipl表达对内质网应激条件下肝癌细胞周期和凋亡起重要调控作用。

英文摘要：

Objective To investigate the role of miR-221/222 in inhibiting endoplasmic reticulum stress-induced human hepatocarcinoma cells apoptosis. Method miR-221/222 mimics and inhibitors were used to mimic or block the function of endogenous miR-221/222 respectively. Western blot and flow cytometry were used to test the effects of miR-221/222 on cell cycle and apoptosis under endoplasmic reticulum stress in human hepatocellular carcinoma cells. Results Endoplasmic reticulum stress resulted in miR-221/222 down-regulation in human hepatocellular carcinoma cells, miR-221/222 mimics and inhibitors inhibited and promoted respectively endoplasmic reticulum stress-mediated p27Kipl induction. Moreover, p27Kipl suppression not only resulted in reduction in the fraction of GI phase cells, but also promoted the endoplasmic reticulum stress-mediated apoptosis in human hepatocellular carcinoma cells. Conclusions miR-221/222 were downregulated by endoplasmic reticulum stress in human hepatocellular carcinoma cells, which subsequently protected human hepatocellular carcinoma cells against endoplasmic reticulum stress-induced apoptosis through p27^Kipl regulation.