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  1. 050 医学部, 大学院医学系研究科
  2. 0501 学術論文

Specific mtDNA Mutations in Mouse Carcinoma Cells Suppress Their Tumor Formation via Activation of the Host Innate Immune System

http://hdl.handle.net/10091/00019828
34fb5b48-792f-42e2-a67b-39dc23dd18c7
名前 / ファイル ライセンス アクション
Specific_mtDNA_Mutations_Mouse_Carcinoma_Cells.pdf Specific_mtDNA_Mutations_Mouse_Carcinoma_Cells.pdf (585.8 kB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2017-09-20
タイトル
言語 en
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
言語 eng
資源タイプ
資源 http://purl.org/coar/resource_type/c_6501
タイプ journal article
著者 Imanishi, Hirotake

× Imanishi, Hirotake

WEKO 104001

en Imanishi, Hirotake

Search repository
Takibuchi, Gaku

× Takibuchi, Gaku

WEKO 104002

en Takibuchi, Gaku

Search repository
Kobayashi, Toshihiko

× Kobayashi, Toshihiko

WEKO 104003

en Kobayashi, Toshihiko

Search repository
Ishikawa, Kaori

× Ishikawa, Kaori

WEKO 104004

en Ishikawa, Kaori

Search repository
Nakada, Kazuto

× Nakada, Kazuto

WEKO 104005

en Nakada, Kazuto

Search repository
Mori, Masayuki

× Mori, Masayuki

WEKO 104006

en Mori, Masayuki

Search repository
Kikkawa, Yoshiaki

× Kikkawa, Yoshiaki

WEKO 104007

en Kikkawa, Yoshiaki

Search repository
Takenaga, Keizo

× Takenaga, Keizo

WEKO 104008

en Takenaga, Keizo

Search repository
Toyama-Sorimachi, Noriko

× Toyama-Sorimachi, Noriko

WEKO 104009

en Toyama-Sorimachi, Noriko

Search repository
Hayashi, Jun-Ichi

× Hayashi, Jun-Ichi

WEKO 104010

en Hayashi, Jun-Ichi

Search repository
信州大学研究者総覧へのリンク
氏名 Mori, Masayuki
URL http://soar-rd.shinshu-u.ac.jp/profile/ja.OpSCZafV.html
出版者
出版者 PUBLIC LIBRARY SCIENCE
引用
内容記述タイプ Other
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
抄録
内容記述タイプ Abstract
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)
内容記述タイプ Other
内容記述 Article
ISSN
収録物識別子タイプ PISSN
収録物識別子 1932-6203
PubMed
関連識別子
識別子タイプ PMID
関連識別子 https://pubmed.ncbi.nlm.nih.gov/24098752
関連名称
関連名称 24098752
DOI
関連識別子
識別子タイプ DOI
関連識別子 https://doi.org/10.1371/journal.pone.0075981
関連名称
関連名称 10.1371/journal.pone.0075981
権利
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
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
WoS
表示名 Web of Science
URL http://gateway.isiknowledge.com/gateway/Gateway.cgi?&GWVersion=2&SrcAuth=ShinshuUniv&SrcApp=ShinshuUniv&DestLinkType=FullRecord&DestApp=WOS&KeyUT=000325423500122
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