目的:探讨人剪接型X盒结合蛋白1(X-box binding protein1spliced,XBP1S)对肝癌HepG2细胞增殖和凋亡的影响。方法:应用衣霉素(tunicamycin,Tm)和毒胡萝卜素(thapsigargin,Tg)建立HepG2细胞的内质网应激(endoplasmic reticulum stress,ERS)模型。将XBP1S真核表达载体pcDNA3.1(-)-XBP1S和靶向XBP1S的RNA干扰质粒pSUPER-XBP1S转染HepG2细胞,MTT法检测细胞的增殖能力,荧光显微镜下观察细胞的形态学变化,FCM法检测细胞凋亡率,Western印迹法检测caspase12的表达。结果:转染pSUPER-XBP1S可有效抑制细胞增殖,而转染pcDNA3.1(-)-XBP1S可促进细胞增殖。荧光显微镜下可见Tm处理组细胞出现细胞凋亡的形态学改变,进一步下调XBP1S的表达可使这一改变增强。对照组、Tm组、Tm+pSUPER-XBP1S转染组和Tm+pcDNA3.1(-)-XBP1S转染组细胞的凋亡率分别为5.21%、41.51%、52.15%和35.87%,差异有统计学意义(P<0.05)。HepG2细胞中caspase12的表达,Tm组高于对照组,Tm+pSUPER-XBP1S转染组高于Tm组,Tm+pcDNA3.1(-)-XBP1S转染组低于Tm组。结论:XBP1S可以促进肝癌HepG2细胞增殖,抑制或促进XBP1S表达可调节ERS介导的细胞凋亡。 Objective: To investigate the effect of XBP1S on proliferation and apoptosis of hepatocellular carcinoma HepG2 cells. Methods: The endoplasmic reticulum stress (ERS) model of HepG2 cells was established by using tunicamycin (Tm) and thapsigargin (Tg). The XBP1S eukaryotic expression vector pcDNA3.1 (-) - XBP1S and the XBP1S RNA interference plasmid pSUPER-XBP1S were transfected into HepG2 cells. The proliferation of HepG2 cells was detected by MTT assay. The morphological changes of cells were observed under fluorescence microscope. The rate of apoptosis was detected and the expression of caspase12 was detected by Western blotting. Results: Transfection of pSUPER-XBP1S could effectively inhibit cell proliferation, while transfection of pcDNA3.1 (-) - XBP1S promoted cell proliferation. Fluorescence microscopy showed Tm-treated cells showed morphological changes of apoptosis, further down-regulation of XBP1S expression can make this change enhanced. The apoptosis rates of control group, Tm group, Tm + pSUPER-XBP1S transfection group and Tm + pcDNA3.1 (-) - XBP1S transfection group were 5.21%, 41.51%, 52.15% and 35.87%, respectively Significance (P <0.05). The expression of caspase 12 in HepG2 cells was higher in Tm group than in Tm + pSUPER-XBP1S transfection group, but lower in Tm + pcDNA3.1 (-) - XBP1S transfection group than in Tm group. Conclusion: XBP1S can promote the proliferation of HepG2 cells and inhibit or promote the expression of XBP1S, which can regulate ERS-mediated apoptosis.