Item type |
学術雑誌論文 / Journal Article(1) |
公開日 |
2017-09-20 |
タイトル |
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タイトル |
Specific mtDNA Mutations in Mouse Carcinoma Cells Suppress Their Tumor Formation via Activation of the Host Innate Immune System |
言語 |
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言語 |
eng |
DOI |
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関連識別子 |
https://doi.org/10.1371/journal.pone.0075981 |
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関連名称 |
10.1371/journal.pone.0075981 |
資源タイプ |
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資源 |
http://purl.org/coar/resource_type/c_6501 |
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タイプ |
journal article |
著者 |
Imanishi, Hirotake
Takibuchi, Gaku
Kobayashi, Toshihiko
Ishikawa, Kaori
Nakada, Kazuto
Mori, Masayuki
Kikkawa, Yoshiaki
Takenaga, Keizo
Toyama-Sorimachi, Noriko
Hayashi, Jun-Ichi
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信州大学研究者総覧へのリンク |
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氏名 |
Mori, Masayuki |
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URL |
http://soar-rd.shinshu-u.ac.jp/profile/ja.OpSCZafV.html |
出版者 |
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出版者 |
PUBLIC LIBRARY SCIENCE |
引用 |
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内容記述 |
PLOS ONE. 8(9):UNSP e75981 (2013) |
書誌情報 |
PLOS ONE
巻 8,
号 9,
p. UNSP e75981,
発行日 2013-09-16
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抄録 |
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内容記述 |
mammalian species, mitochondrial DNA (mtDNA) with pathogenic mutations that induce mitochondrial respiration defects has been proposed to be involved in tumor phenotypes via induction of enhanced glycolysis under normoxic conditions (the Warburg effects). However, because both nuclear DNA and mtDNA control mitochondrial respiratory function, it is difficult to exclude the possible contribution of nuclear DNA mutations to mitochondrial respiration defects and the resultant expression of tumor phenotypes. Therefore, it is important to generate transmitochondrial cybrids sharing the same nuclear DNA background but carrying mtDNA with and without the mutations by using intercellular mtDNA transfer technology. Our previous studies isolated transmitochondrial cybrids and showed that specific mtDNA mutations enhanced tumor progression as a consequence of overproduction of reactive oxygen species (ROS). This study assessed whether mtDNA mutations inducing ROS overproduction always enhance tumor progression. We introduced mtDNA from senescence-accelerated mice P1 (SAMP1) into C57BL/6J (B6) mice-derived Lewis lung carcinoma P29 cells, and isolated new transmitochondrial cybrids (P29mtSAMP1 cybrids) that overproduced ROS. The inoculation of the cybrids into B6 mice unexpectedly showed that mtDNA from SAMP1 mice conversely induced tumor suppression. Moreover, the tumor suppression of P29mtSAMP1 cybrids in B6 mice occurred as a consequence of innate immune responses of the host B6 mice. Enzyme pretreatment experiments of P29mtSAMP1 cybrids revealed that some peptides encoded by mtDNA and expressed on the cell surface of P29mtSAMP1 cybrids induce increased IL-6 production from innate immune cells (dendritic cells) of B6 mice, and mediate augmented inflammatory responses around the tumor-inoculated environment. These observations indicate presence of a novel role of mtDNA in tumor phenotype, and provide new insights into the fields of mitochondrial tumor biology and tumor immunology. |
資源タイプ(コンテンツの種類) |
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内容記述 |
Article |
ISSN |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
1932-6203 |
PubMed |
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関連識別子 |
https://pubmed.ncbi.nlm.nih.gov/24098752 |
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関連名称 |
24098752 |
権利 |
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権利情報 |
© 2013 Imanishi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
出版タイプ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
WoS |
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URL |
http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000325423500122 |