| 摘要: |
| 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(1 μmol/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 1 μmol/L 鱼藤酮干预Caco2细胞48 h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,1 μmol/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。 |
| 关键词: 线粒体 呼吸链复合物Ⅰ 结肠肿瘤 肿瘤转移 细胞迁移 细胞侵袭 活性氧 |
| DOI：10.3724/SP.J.1008.2015.01324 |
| 投稿时间：2015-01-28修订日期：2015-06-02 |
| 基金项目:国家自然科学基金青年基金(81000932),上海市自然科学基金(11ZR1447700). |
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| Effect of inhibiting mitochondrial respiratory chain complex Ⅰ on migration and invasion capacity of colon cancer cell line Caco2 |
| WANG Wei-xingΔ,YUAN YangΔ,LIU Jing-yu,JIANG Xu,YANG Ji-jin* |
(Department of Interventional Radiology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
△Co-first authors.
*Corresponding author.) |
| Abstract: |
| Objective To investigate the effect of inhibiting mitochondrial respiratory chain complex Ⅰ on the migration and invasion capacity of colon cancer cell line Caco2, and to explore the possible molecular mechanism. Methods Human colon cancer cell line Caco2 was treated with 1 μmol/L rotenone in vitro. Then the relative activity of mitochondrial respiratory chain complex Ⅰ was examined by chromatometry, the capacity of cell migration and invasion was determined by transwell assay, and the reactive oxygen species (ROS) level in cells was determined using flow cytometry. Results The activity of mitochondrial respiratory chain complex Ⅰ of Caco2 cells treated with 1 μmol/L rotenone was significantly lower than that of the untreated cells(P<0.01). In addition, Transwell assay showed that the cell migration rate and invasive rate in Caco2 cells treated with rotenone were significantly higher than those in untreated Caco2 cells after 48 h (migrant rate [30.4±1.4]% vs [22.6±1.4]%, invasive rate [20.3±1.0]% vs [15.2±1.3]%, P<0.01). Furthermore, the ROS level in the rotenone treated cells was significantly higher than that in untreated cells ([5.68±0.44]% vs [3.46±0.30]%, P<0.01). Conclusion Our data suggest that inhibiting the activity of mitochondrial respiratory chain complex Ⅰ may promote cell migration and invasion by increasing ROS production in colon cancer cells. |
| Key words: mitochondria respiratory chain complex Ⅰ colon neoplasms neoplasm metastasis cell migration cell invasion reactive oxygen species |
