抑制线粒体复合体Ⅱ诱导线粒体自噬影响细胞增殖的研究（英文）
发布时间：2024-02-01 06:53
线粒体复合体Ⅱ,也被称为琥珀酸脱氢酶,参与线粒体呼吸作用及代谢重编程的调控过程.复合体Ⅱ由4个亚基构成,其突变与肿瘤的发生密切相关.本文探讨复合体Ⅱ与线粒体自噬调控及细胞增殖之间的关系.实验采用复合体Ⅱ的特异性抑制剂TTFA或敲除复合体Ⅱ的B亚基(SDHB)使其功能缺失.结果发现,复合体Ⅱ功能的缺失显著引起线粒体形态的片段化进而发生线粒体自噬,导致线粒体蛋白水平减少,抑制ATP生成;由于线粒体功能受到抑制,细胞葡萄糖消耗及乳酸产生水平增加,并显著抑制细胞的细胞的增殖.综上所述,复合体Ⅱ功能缺失可能通过调控线粒体自噬而影响细胞增殖,从而在肿瘤发生中起重要作用.
【文章页数】：8 页
【文章目录】：
1 Materials and Methods
1.1 Plasmids and other reagents
1.2 Cells and culture
1.3 Western-blotting
1.4 Immunofluorescence
1.5 Statistical analysis
2 Results
2.1 Inhibition of complex II induces mitochondria fragmentation and reduces mitochondrial proteins
2.2 Inhibition of complex II induces mitophagy
2.3 SDHB knockdown regulates cell proliferation
3 Discussion
本文编号：3891733
【文章页数】：8 页
【文章目录】：
1 Materials and Methods
1.1 Plasmids and other reagents
1.2 Cells and culture
1.3 Western-blotting
1.4 Immunofluorescence
1.5 Statistical analysis
2 Results
2.1 Inhibition of complex II induces mitochondria fragmentation and reduces mitochondrial proteins
2.2 Inhibition of complex II induces mitophagy
2.3 SDHB knockdown regulates cell proliferation
3 Discussion
本文编号：3891733
本文链接：https://www.wllwen.com/projectlw/swxlw/3891733.html
