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线粒体基因组突变:体细胞向癌细胞转化的触发因素。

Mutation of mitochondria genome: trigger of somatic cell transforming to cancer cell.

作者信息

Jianping Du

机构信息

Department of Oncology, Anhui Provincial Hospital, 9 Lujiang Road, Hefei 230001, PR China.

出版信息

Int Arch Med. 2010 Feb 5;3(1):4. doi: 10.1186/1755-7682-3-4.

Abstract

Nearly 80 years ago, scientist Otto Warburg originated a hypothesis that the cause of cancer is primarily a defect in energy metabolism. Following studies showed that mitochondria impact carcinogenesis to remodel somatic cells to cancer cells through modifying the genome, through maintenance the tumorigenic phenotype, and through apoptosis. And the Endosymbiotic Theory explains the origin of mitochondria and eukaryotes, on the other hands, the mitochondria also can fall back. Compared to chromosome genomes, the mitochondria genomes were not restricted by introns so they were mutated(fall back) easy. The result is that mitochondria lose function and internal environment of somatic cell become acid and evoked chromosome genomes to mutate, in the end somatic cells become cancer cells. It is the trigger of somatic cell transforming to cancer cell that mitochondria genome happen mutation and lose function.

摘要

近80年前,科学家奥托·瓦尔堡提出了一种假说,即癌症的起因主要是能量代谢缺陷。后续研究表明,线粒体通过修饰基因组、维持致瘤表型以及诱导凋亡来影响致癌作用,从而将体细胞重塑为癌细胞。另一方面,内共生理论解释了线粒体和真核生物的起源,线粒体也会退化。与染色体基因组相比,线粒体基因组不受内含子限制,因此更容易发生突变(退化)。结果是线粒体功能丧失,体细胞内部环境变酸,进而诱发染色体基因组发生突变,最终体细胞变成癌细胞。线粒体基因组发生突变并丧失功能是体细胞转变为癌细胞的触发因素。

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本文引用的文献

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Mitochondria in cancer cells: what is so special about them?癌细胞中的线粒体:它们有何特别之处?
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