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Enhanced glycolysis induced by mtDNA mutations does not regulate metastasis
Author(s) -
Ishikawa Kaori,
Hashizume Osamu,
Koshikawa Nobuko,
Fukuda Sayaka,
Nakada Kazuto,
Takenaga Keizo,
Hayashi Jun-Ichi
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.09.024
Subject(s) - glycolysis , mitochondrial dna , metastasis , mutation , chemistry , genetics , biology , cancer research , microbiology and biotechnology , biochemistry , metabolism , gene , cancer
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 P29mtΔ cybrids, possessed mtDNA with a G13997A mutation from highly metastatic carcinoma A11 cells and mtDNA with a 4696 bp deletion mutation, respectively. The P29mtΔ 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.