Reversible regulation of metastasis by ROS-generating mtDNA mutations
Reversible regulation of metastasis by ROS-generating mtDNA mutations
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DOI：
10.1016/j.mito.2008.07.006
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发表时间：
2008-09-01
期刊：
影响因子：
4.4
通讯作者：
Hayashi, Jun-Ichi
中科院分区：
文献类型：
--
作者：
Ishikawa, Kaori;Koshikawa, Nobuko;Hayashi, Jun-Ichi
mtDNA 突变是否导致致癌转化（正常细胞发展为肿瘤）和恶性进展（肿瘤细胞发展为转移）一直存在争议。为了澄清这个问题，我们创建了跨线粒体杂种，其中 mtDNA 在表达不同转移表型的小鼠肿瘤细胞之间交换。来自高转移性肿瘤细胞的线粒体DNA的ND6基因中的G13997A突变通过活性氧（ROS）的过量产生可逆地控制转移的发展，但不控制肿瘤的发展。 mtDNA 介导的可逆转移控制揭示了 mtDNA 的新功能，并表明 ROS 清除剂可能在抑制转移方面具有治疗效果。 (c) 2008 年 Elsevier B.V. 和线粒体研究协会。版权所有。
It has been controversial whether mtDNA mutations are responsible for oncogenic transformation (normal cells to develop tumors), and for malignant progression (tumor cells to develop metastases). To clarify this issue, we created trans-mitochondrial cybrids with mtDNA exchanged between mouse tumor cells that express different metastatic phenotypes. The G13997A mutation in the ND6 gene of mtDNA from high metastatic tumor cells reversibly controlled development of metastases by overproduction of reactive oxygen species (ROS), but did not control development of tumors. The mtDNA-mediated reversible control of metastasis reveals a novel function of mtDNA, and suggests that ROS scavengers may be therapeutically effective in suppressing metastasis. (c) 2008 Elsevier B.V. and Mitochondria Research Society. All rights reserved.