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线粒体DNA(mitochondrialDNA,mtDNA)编码参与氧化磷酸化和ATP生成所必需的多肽,与核基因组相比,mtDNA的突变率非常高,加之本身缺乏有效的损伤修复系统,所以mtDNA被认为与肿瘤发生有密切的关系。mtDNA的编码区内缺乏内含子,提示大多数突变发生于此编码序列,突变的积累可能导致肿瘤的发生。mtDNA的表达改变可能是癌细胞的一个特性。近年来有关线粒体基因组不稳定性(mitochondrialgenomeinstability,mtGI)及mtDNA与核基因组整合研究,尤其针对实体瘤的研究逐渐增多。肿瘤mtDNA的研究将成为对实体肿瘤研究的又一项重要课题。本文将对线粒体基因组的突变、表达异常、整合和不稳定性与实体性肿瘤发病机制的关系,尤其是在近年所取得的进展作一综述。
Mitochondrial DNA (mtDNA) encodes the polypeptide involved in oxidative phosphorylation and ATP production. Compared with the nuclear genome, the mtDNA mutation rate is very high, and the lack of effective damage repair system itself, so mtDNA is considered with the tumor close relationship. The lack of introns in the coding region of mtDNA suggests that most mutations occur in this coding sequence and the accumulation of mutations may lead to tumorigenesis. Changes in mtDNA expression may be a feature of cancer cells. In recent years, mitochondrial genome instability (mitochondrialgenomeinstability, mtGI) and mtDNA and nuclear genome integration studies, especially for solid tumors research is increasing. The study of tumor mtDNA will be another important topic in the study of solid tumors. This article reviews the relationship between mitochondrial genome mutations, abnormal expression, integration and instability with the pathogenesis of solid tumors, especially the progress made in recent years.