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Nrf2 activation drive macrophages polarization and cancer cell epithelial-mesenchymal transition during interaction

https://tokushima-u.repo.nii.ac.jp/records/2007486
https://tokushima-u.repo.nii.ac.jp/records/2007486
bb2154ce-00eb-4cf4-b56d-c79cb9f008e0
名前 / ファイル ライセンス アクション
ccs_16_54.pdf ccs_16_54.pdf (2.68 MB)
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Item type 文献 / Documents(1)
公開日 2020-12-07
アクセス権
アクセス権 open access
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版社版DOI
関連識別子 https://doi.org/10.1186/s12964-018-0262-x
関連名称 10.1186/s12964-018-0262-x
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
タイトル
タイトル Nrf2 activation drive macrophages polarization and cancer cell epithelial-mesenchymal transition during interaction
著者 Feng, Rui

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en Feng, Rui

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森根, 裕二

× 森根, 裕二

WEKO 193
徳島大学 教育研究者総覧 121751/profile-ja.html
e-Rad 60398021

ja 森根, 裕二
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ja-Kana モリネ, ユウジ

en Morine, Yuji

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池本, 哲也

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WEKO 265
徳島大学 教育研究者総覧 157341/profile-ja.html
e-Rad 20398019

ja 池本, 哲也
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ja-Kana イケモト, テツヤ

en Ikemoto, Tetsuya

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居村, 暁

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WEKO 1266
e-Rad 90380021

ja 居村, 暁
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ja-Kana イムラ, サトル

en Imura, Satoru

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岩橋, 衆一

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e-Rad 30531751

ja 岩橋, 衆一
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ja-Kana イワハシ, シュウイチ

en Iwahashi, Shuichi

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齋藤, 裕

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徳島大学 教育研究者総覧 277637/profile-ja.html
e-Rad 50548675

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ja-Kana サイトウ, ユウ

en Saitou, Yu

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島田, 光生

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徳島大学 教育研究者総覧 82712/profile-ja.html
e-Rad 10216070

ja 島田, 光生
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ja-Kana シマダ, ミツオ

en Shimada, Mitsuo

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抄録
内容記述 Background: The M2 phenotype of tumor-associated macrophages (TAM) inhibits the anti-tumor inflammation, increases angiogenesis and promotes tumor progression. The transcription factor Nuclear Factor (erythroid-derived 2)-Like 2 (Nrf2) not only modulates the angiogenesis but also plays the anti-inflammatory role through inhibiting pro-inflammatory cytokines expression; however, the role of Nrf2 in the cancer cell and macrophages interaction is not clear.
Methods: Hepatocellular carcinoma cells (Hep G2 and Huh 7) and pancreatic cancer cells (SUIT2 and Panc-1) were co-cultured with monocytes cells (THP-1) or peripheral blood monocytes derived macrophages, then the phenotype changes of macrophages and epithelial-mesenchymal transition of cancer cells were detected. Also, the role of Nrf2 in cancer cells and macrophages interaction were investigated.
Results: In this study, we found that cancer cells could induce an M2-like macrophage characterized by up-regulation of CD163 and Arg1, and down-regulation of IL-1b and IL-6 through Nrf2 activation. Also, Nrf2 activation of macrophages promoted VEGF expression. The Nrf2 activation of macrophages correlated with the reactive oxygen species induced by cancer cells derived lactate. Cancer cells educated macrophages could activate Nrf2 of the cancer cells, in turn, to increase cancer cells epithelial-mesenchymal transition (EMT) through paracrine VEGF. These findings suggested that Nrf2 played the important role in the cancer cells and macrophages interaction.
Conclusions: Macrophage Nrf2 activation by cancer cell-derived lactate skews macrophages polarization towards an M2-like phenotype and educated macrophages activate Nrf2 of the cancer cells to promote EMT of cancer cells. This study provides a new understanding of the role of Nrf2 in the cancer cell and TAM interaction and suggests a potential therapeutic target.
キーワード
主題 Nuclear factor (erythroid-derived 2)-like 2
キーワード
主題 Tumor-associated macrophage
キーワード
主題 Hepatocellular carcinoma
キーワード
主題 Pancreatic cancer
キーワード
主題 Epithelial-mesenchymal transition
書誌情報 en : Cell Communication and Signaling

巻 16, p. 54, 発行日 2018-09-04
収録物ID
収録物識別子タイプ ISSN
収録物識別子 1478811X
出版者
出版者 Springer Nature
出版者
出版者 BioMed Central
権利情報
権利情報 © The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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識別子 351465
言語
言語 eng
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