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A novel function of mtDNA: its involvement in metastasis
Author(s) -
Ishikawa Kaori,
Hayashi JunIchi
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2010.05616.x
Subject(s) - mitochondrial dna , metastasis , phenotype , reactive oxygen species , mutation , cancer research , biology , overproduction , function (biology) , mitochondrion , malignant transformation , gene , transformation (genetics) , cancer , microbiology and biotechnology , genetics
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 transmitochondrial 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). 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.