期刊
MITOCHONDRION
卷 8, 期 4, 页码 339-344出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2008.07.006
关键词
mtDNA mutation; ROS overproduction; Nuclear-gene regulation; Metastasis; mtDNA transfer technology
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.
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