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| ファイル | 記述 | サイズ | フォーマット | |
|---|---|---|---|---|
| s41467-018-03966-7.pdf | 1.21 MB | Adobe PDF | 見る/開く |
| タイトル: | Snail promotes ovarian cancer progression by recruiting myeloid-derived suppressor cells via CXCR2 ligand upregulation |
| 著者: | Taki, Mana    https://orcid.org/0000-0002-1540-0985 (unconfirmed)Abiko, Kaoru Baba, Tsukasa Hamanishi, Junzo https://orcid.org/0000-0002-7750-0623 (unconfirmed)Yamaguchi, Ken Murakami, Ryusuke Yamanoi, Koji https://orcid.org/0000-0002-1240-5422 (unconfirmed)Horikawa, Naoki Hosoe, Yuko Nakamura, Eijiro Sugiyama, Aiko Mandai, Masaki Konishi, Ikuo Matsumura, Noriomi |
| 著者名の別形: | 滝, 真奈 安彦, 郁 馬場, 長 |
| キーワード: | Cancer microenvironment Ovarian cancer Tumour immunology |
| 発行日: | 27-Apr-2018 |
| 出版者: | Springer Nature |
| 誌名: | Nature Communications |
| 巻: | 9 |
| 論文番号: | 1685 |
| 抄録: | Snail is a major transcriptional factor that induces epithelial-mesenchymal transition (EMT). In this study, we explore the effect of Snail on tumor immunity. Snail knockdown in mouse ovarian cancer cells suppresses tumor growth in immunocompetent mice, associated with an increase of CD8+ tumor-infiltrating lymphocytes and a decrease of myeloid-derived suppressor cells (MDSCs). Snail knockdown reduces the expression of CXCR2 ligands (CXCL1 and CXCL2), chemokines that attract MDSCs to the tumor via CXCR2. Snail upregulates CXCR ligands through NF-kB pathway, and most likely, through direct binding to the promoters. A CXCR2 antagonist suppresses MDSC infiltration and delays tumor growth in Snail-expressing mouse tumors. Ovarian cancer patients show elevated serum CXCL1/2, which correlates with Snail expression, MDSC infiltration, and short overall survival. Thus, Snail induces cancer progression via upregulation of CXCR2 ligands and recruitment of MDSCs. Blocking CXCR2 represents an immunological therapeutic approach to inhibit progression of Snail-high tumors undergoing EMT. |
| 記述: | 卵巣がんの免疫回避のメカニズムを解明 --ケモカイン阻害剤が有望な新規治療薬となる可能性を提示--. 京都大学プレスリリース. 2018-05-02. |
| 著作権等: | © The Author(s) 2018 This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
| URI: | http://hdl.handle.net/2433/230942 |
| DOI(出版社版): | 10.1038/s41467-018-03966-7 |
| PubMed ID: | 29703902 |
| 関連リンク: | https://www.kyoto-u.ac.jp/ja/research-news/2018-05-02-2 |
| 出現コレクション: | 学術雑誌掲載論文等 |
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