CAJ | 학술논문

目的:探讨人剪接型X盒结合蛋白1(X-box binding protein 1 spliced,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XBPlS真核表达载体pcDNA3.1(-)-XBPIS和靶向XBPlS的RNA干扰质粒pSUPER-XBPIS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XBPlS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(-)-XBPIS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.
목적:탐토인전접형X합결합단백1(X-box binding protein 1 spliced,XBP1S)대간암HepG2세포증식화조망적영향.방법:응용의매소(tunicamycin,Tm)화독호라복소(thapsigargin,Tg)건립HepG2세포적내질망응격(endoplasmic reticulum stress,ERS)모형.장XBPlS진핵표체재체pcDNA3.1(-)-XBPIS화파향XBPlS적RNA간우질립pSUPER-XBPIS전염HepG2세포,MTT법검측세포적증식능력,형광현미경하관찰세포적형태학변화,FCM법검측세포조망솔,Western인적법검측caspase12표체.결과:전염pSUPER-XBP1S가유효억제세포증식,이전염pcDNA3.1(-)-XBP1S가촉진세포증식.형광현미경하가견Tm처리조세포출현세포조망적형태학개변,진일보하조XBPlS적표체가사저일개변증강.대조조、Tm조、Tm+pSUPER-XBP1S전염조화Tm+pcDNA3.1(-)-XBPIS전염조세포적조망솔분별위5.21%、41.51%、52.15%화35.87%,차이유통계학의의(P＜0.05).HepG2세포중caspase12적표체,Tm조고우대조조,Tm+pSUPER-XBP1S전염조고우Tm조,Tm+pcDNA3.1(-)-XBP1S전염조저우Tm조.결론:XBP1S가이촉진간암HepG2세포증식,억제혹촉진XBP1S표체가조절ERS개도적세포조망.