CAJ | 학술논문

目的探讨亚硒酸钠杀伤结肠癌肿瘤细胞的潜在机制.方法应用MTS方法和DCFH-DA法分别检测亚硒酸钠对人结肠癌细胞系HCT116存活率和细胞内活性氧水平的影响,同时应用小分子干扰RNA片段研究JNK1和p53在亚硒酸钠介导的细胞死亡过程中的作用.结果实验结果表明亚硒酸钠通过显著提高HCT116细胞内的活性氧水平,致使细胞发生氧化应激,激活应激相关蛋白JNK1和p53,从而达到杀伤肿瘤细胞的作用.结论亚硒酸钠能有效杀伤结肠癌肿瘤细胞,同时JNK1和p53在亚硒酸钠介导的细胞死亡过程中发挥了重要作用.
목적 탐토아서산납살상결장암종류세포적잠재궤제.방법 응용MTS방법화DCFH-DA법분별검측아서산납대인결장암세포계HCT116존활솔화세포내활성양수평적영향,동시응용소분자간우RNA편단연구JNK1화p53재아서산납개도적세포사망과정중적작용.결과 실험결과표명아서산납통과현저제고HCT116세포내적활성양수평,치사세포발생양화응격,격활응격상관단백JNK1화p53,종이체도살상종류세포적작용.결론 아서산납능유효살상결장암종류세포,동시JNK1화p53재아서산납개도적세포사망과정중발휘료중요작용.
Objective To investigate the inhibition mechanism of sodium selenite on HCT116 cells.Methods In the present study,we explored the cytotoxicity induced by sodium selenite and the underlying mechanism by MTS assay,WesternBlot,and small RNA interference technique.Results It was found that the sodium selenite at 5uM concentration could indeed reduce the viability of colon cancer cell line HCT116 by a large margin through increasing the generation of reactive oxygen species (ROS),and that the increased levels of ROS could activate c-Jun Nh2-terninal kinase 1 (JNK1).Additionally,knockdown expression of JNK1 or p53 by using RNAi attenuated the cytotoxicity induced by sodium selenite,indicating that both of JNK1 and p53 are required in the process of cell death induced by sodium selenite.Conclusion The sodium selenite could induces cell death in HCT116 through oxidative stress by involvement of JNK1 and p53,both of which play a critical role in toxicity of sodium selenite.