CAJ | 학술논문

目的:探讨新型组蛋白去乙酰化酶抑制剂LBH589或联合多烯紫杉醇(DTX)对人卵巢癌OVCAR-3细胞增殖和凋亡的影响.方法:采用不同浓度LBH589、DTX或两者联合处理OVCAR-3细胞,用四甲基偶氮唑蓝(MTT)法检测细胞增殖活力,台盼兰、吖啶橙溴化乙啶(AO/EB)双染色法检测细胞凋亡;Western blot检测聚腺苷二磷酸核糖聚合酶(PARP)、caspase-3、cas?pase-7、bcl-2、bax蛋白水平.结果:LBH589、DTX均能抑制OVCAR-3细胞增殖,诱导凋亡,小剂量LBH589联合DTX作用更强.经Calcusyn软件分析证明两者联合具有明显的协同作用.Western blot检测发现caspsae-3、PARP-85kD剪切蛋白增加,bax表达增加,bcl-2表达减少.caspase-7无明显变化.结论:LBH589、DTX能抑制OVCAR-3细胞增殖,诱导凋亡,两者联合有明显的协同作用.
목적:탐토신형조단백거을선화매억제제LBH589혹연합다희자삼순(DTX)대인란소암OVCAR-3세포증식화조망적영향.방법:채용불동농도LBH589、DTX혹량자연합처리OVCAR-3세포,용사갑기우담서람(MTT)법검측세포증식활력,태반란、아정등추화을정(AO/EB)쌍염색법검측세포조망;Western blot검측취선감이린산핵당취합매(PARP)、caspase-3、cas?pase-7、bcl-2、bax단백수평.결과:LBH589、DTX균능억제OVCAR-3세포증식,유도조망,소제량LBH589연합DTX작용경강.경Calcusyn연건분석증명량자연합구유명현적협동작용.Western blot검측발현caspsae-3、PARP-85kD전절단백증가,bax표체증가,bcl-2표체감소.caspase-7무명현변화.결론:LBH589、DTX능억제OVCAR-3세포증식,유도조망,량자연합유명현적협동작용.
This work aimed to investigate the effects of LBH589, a novel histone deacetylase (HDAC) inhibitor, alone or in combination with docetaxel (DTX) on the proliferation and apoptosis of the human ovarian cancer cell line OVCAR-3. Methods: OVCAR-3 cells were treated with LBH589, DTX, or a combination of both at various concentrations. The proliferation capacity, apoptosis rate, and reversal of drug resistance were evaluated by MTT assay. The apoptotic rate of the cells was detected using trypan blue and acridine orange/ethidium bromide double-staining methods. The expression of proteins such as poly-ADP-ribose polymerase (PARP), caspase-3, caspase-7, bel-2, and bax were analyzed by Western blot analysis. Results:Synergistic cytotoxicity was observed in the combination therapy using low doses of LBH589 and DTX against OVCAR-3 cells. The synergistic effect was confirmed by Calcusyn software analysis. OVCAR-3 cells apparently increased in number in the combination therapy than in either LBH589 or DTX therapy alone. Western blot analysis showed that the expression of cleaved PARP-85KD, caspase-3, and bax increased, whereas bcl-2 was downregulated. Conclusion: LBH589 and DTX in vitro can significantly inhibit the proliferation of human ovarian cancer cell line OVCAR-3 and induce cell apoptosis of these cells. Combined LBH589 and DTX treatment against drug-resistant OVCAR-3 cells resulted in a synergistic effect of increased sensitivity to chemotherapy.