Enhanced glycolysis induced by mtDNA mutations does not regulate metastasis
Enhanced glycolysis induced by mtDNA mutations does not regulate metastasis
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DOI：
10.1016/j.febslet.2008.09.024
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发表时间：
2008-10-15
期刊：
影响因子：
3.5
通讯作者：
Hayashi, Jun-Ichi
中科院分区：
文献类型：
--
作者：
Ishikawa, Kaori;Hashizume, Osamu;Hayashi, Jun-Ichi
我们使用mtDNA转移技术解决了由mtDNA突变引起的糖酵解增强是否独立地诱导肿瘤细胞转移的问题。结果表明，P29mtA11和P29mtDelta胞质杂交体的mtDNA分别具有来自高转移癌细胞A11的G13997A突变和4696bp缺失突变，这两种胞质杂交体具有与低转移癌细胞P29相同的核背景。P29mtD胞质杂交体表达增强的糖酵解，但不表达ROS过量产生和高转移潜力，而P29mtA11胞质杂交体显示增强的糖酵解，ROS过量产生和高转移潜力。因此，单独增强的糖酵解不会诱导胞质杂交体中的转移。
We addressed the issue of whether enhanced glycolysis caused by mtDNA mutations independently induces metastasis in tumor cells using mtDNA transfer technology. The resultant trans-mitochondrial cybrids sharing the same nuclear background of poorly metastatic carcinoma P29 cells, P29mtA11 and P29mt Delta cybrids, possessed mtDNA with a G13997A mutation from highly metastatic carcinoma A11 cells and mtDNA with a 4696 bp deletion mutation, respectively. The P29mtD cybrids expressed enhanced glycolysis, but did not express ROS overproduction and high metastatic potential, whereas P29mtA11 cybrids showed enhanced glycolysis, ROS overproduction, and high metastatic potential. Thus, enhanced glycolysis alone does not induce metastasis in the cybrids.