Department Of Pharmacological Sciences & Proteomics Center School Of Medicine, Stony Brook University, Stony Brook, NY 11794-8651, USA.
J Bioenerg Biomembr. 2012 Dec;44(6):619-22. doi: 10.1007/s10863-012-9465-9.
Mitochondria have an essential role in powering cells by generating ATP following the metabolism of pyruvate derived from glycolysis. They are also the major source of generating reactive oxygen species (ROS), which have regulatory roles in cell death and proliferation. Mutations in mitochondrial DNA (mtDNA) and dysregulation of mitochondrial metabolism have been frequently described in human tumors. Although the role of oxidative stress as the consequence of mtDNA mutations and/or altered mitochondrial functions has been demonstrated in carciongenesis, a causative role of mitochondria in tumor progression has only been demonstrated recently. Specifically, the subject of this mini-review focuses on the role of mitochondria in promoting cancer metastasis. Cancer relapse and the subsequent spreading of cancer cells to distal sites are leading causes of morbidity and mortality in cancer patients. Despite its clinical importance, the underlying mechanisms of metastasis remain to be elucidated. Recently, it was demonstrated that mitochondrial oxidative stress could actively promote tumor progression and increase the metastatic potential of cancer cells. The purpose of this mini-review is to summarize current investigations of the roles of mitochondria in cancer metastasis. Future development of diagnostic and therapeutic strategies for patients with advanced cancer will benefit from the new knowledge of mitochondrial metabolism in epithelial cancer cells and the tumor stroma.
线粒体在线粒体 DNA（mtDNA）突变和线粒体代谢失调在人类肿瘤中经常被描述。尽管 mtDNA 突变和/或改变的线粒体功能导致氧化应激的作用在致癌作用中已经得到证实，但线粒体在肿瘤进展中的因果作用直到最近才被证实。具体来说，本综述的主题侧重于线粒体在促进癌症转移中的作用。癌症复发和随后的癌细胞转移到远处部位是癌症患者发病率和死亡率的主要原因。尽管具有临床重要性，但转移的潜在机制仍有待阐明。最近，已经证明线粒体氧化应激可以积极促进肿瘤进展并增加癌细胞的转移潜力。本综述的目的是总结线粒体在癌症转移中的作用的当前研究。对晚期癌症患者的诊断和治疗策略的未来发展将受益于上皮癌细胞和肿瘤基质中线粒体代谢的新知识。
