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Deregulated Mitochondrial DNA in Diseases.
DNA and Cell Biology ( IF 2.6 ) Pub Date : 2020-07-30 , DOI: 10.1089/dna.2019.5220
Ngoc Ngo Yen Nguyen 1, 2 , Sung Soo Kim 2, 3 , Yong Hwa Jo 2, 3
Affiliation  

Mitochondria play various important roles in energy production, metabolism, and apoptosis. Mitochondrial dysfunction caused by alterations in mitochondrial DNA (mtDNA) can lead to the initiation and progression of cancers and other diseases. These alterations include mutations and copy number variations. Especially, the mutations in D-loop, MT-ND1, and MT-ND5 affect mitochondrial functions and are widely detected in various cancers. Meanwhile, several other mutations have been correlated with muscular and neuronal diseases, especially MT-TL1 is deeply related. These pieces of evidence indicated mtDNA alterations in diseases show potential as a novel therapeutic target. mtDNA repair enzymes are the target for delaying or stalling the mtDNA damage-induced cancer progression and metastasis. Moreover, some mutations reveal a prognosis ability of the drug resistance. Current efforts aim to develop mitochondrial transplantation technique as a direct cure for deregulated mitochondria-associated diseases. This review summarizes the implications of mitochondrial dysfunction in cancers and other pathologies; and discusses the relevance of mitochondria-targeted therapies, along with their contribution as potential biomarkers.

中文翻译:

疾病中线粒体DNA失控。

线粒体在能量产生,代谢和凋亡中起着各种重要作用。由线粒体DNA(mtDNA)改变引起的线粒体功能障碍可导致癌症和其他疾病的发生和发展。这些改变包括突变和拷贝数变异。尤其是,D环,MT-ND1MT-ND5中的突变会影响线粒体功能,并在各种癌症中被广泛发现。同时,其他一些突变也与肌肉和神经元疾病有关,尤其是MT-TL1是密切相关的。这些证据表明,疾病中的mtDNA改变显示出作为新型治疗靶点的潜力。mtDNA修复酶是延迟或延缓mtDNA损伤诱导的癌症进展和转移的靶标。此外,一些突变揭示了耐药性的预后能力。当前的努力旨在开发线粒体移植技术,以直接治愈线粒体相关疾病。这篇综述总结了线粒体功能障碍在癌症和其他病理学中的意义。并讨论了针对线粒体的疗法的相关性及其作为潜在生物标志物的贡献。
更新日期:2020-08-04
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