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目的探讨抑制线粒体呼吸链复合物Ⅰ活性对结肠癌细胞Caco2迁移侵袭能力的影响及其可能的机制。方法体外培养的Caco2给予线粒体呼吸链复合物Ⅰ活性抑制物鱼藤酮处理(1μmol/L),采用比色法检测线粒体呼吸链复合物Ⅰ的活性;通过Transwell小室实验检测Caco2细胞迁移、侵袭能力;通过流式细胞术检测细胞内活性氧(ROS)水平。结果 1μmol/L鱼藤酮干预Caco2细胞48h后,胞内线粒体呼吸链复合物Ⅰ活性低于未干预组(P<0.01);Transwell实验结果显示,1μmol/L鱼藤酮干预组细胞的迁移率(30.4±1.4)%、侵袭率(20.3±1.0)%均高于未干预组Caco2细胞的迁移率(22.6±1.4)%和侵袭率(15.2±1.3)%,差异均有统计学意义(P<0.01,P<0.05);鱼藤酮干预组Caco2细胞内ROS水平(5.68±0.44)%高于未干预组(3.46±0.30)%,差异有统计学意义(P<0.01)。结论抑制线粒体呼吸链复合物Ⅰ活性可能通过增加胞内ROS水平的方式增强结肠癌细胞的迁移侵袭能力。
Objective To investigate the effects of mitochondrial respiratory chain complex Ⅰ on Caco2 migration and invasion in colon cancer cells and its possible mechanism. Methods Caco2 was treated with rotenone (1μmol / L), an inhibitor of respiratory chain complex I, and the activity of mitochondrial respiratory chain complex I was detected by colorimetric assay. The migration and invasion ability of Caco2 cells were detected by Transwell chamber assay. Flow cytometry was used to detect intracellular reactive oxygen species (ROS) levels. Results After transfection with 1 μmol / L rotenone for 48 h, the intracellular activity of mitochondrial respiratory chain I was lower than that of the untreated group (P <0.01). The results of Transwell assay showed that the cell migration rate was significantly higher in the group treated with 1 μmol / L rotenone (30.4 ± 1.4 ) And invasive rate (20.3 ± 1.0)% were significantly higher than those in untreated Caco2 cells (22.6 ± 1.4)% and invasive rate (15.2 ± 1.3)%, respectively <0.05). The level of ROS in Caco2 cells treated with rotenone was (5.68 ± 0.44)% higher than that in the untreated group (3.46 ± 0.30)%, the difference was statistically significant (P <0.01). Conclusion Inhibition of mitochondrial respiratory chain complex I activity may enhance the migration and invasion of colon cancer cells by increasing intracellular ROS levels.