ID | 67227 |
フルテキストURL | |
著者 |
Jiang, Fan
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Chen, Youyi
Department of Breast Surgery, The First Affiliated Hospital, Zhejiang University School of Medicine
Tomonobu, Nahoko
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Kinoshita, Rie
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Komalasari, Ni Luh Gede Yoni
Faculty of Medicine, Udayana University
Kasano-Camones, Carlos Ichiro
Faculty of Science and Technology, Division of Molecular Science, Gunma University
Ninomiya, Kazumi
Faculty of Science and Technology, Division of Molecular Science, Gunma University
Murata, Hitoshi
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Yamamoto, Ken-Ichi
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Gohara, Yuma
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Ochi, Toshiki
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Ruma, I. Made Winarsa
Faculty of Medicine, Udayana University
Sumardika, I. Wayan
Faculty of Medicine, Udayana University
Zhou, Jin
Medical Oncology Department of Gastrointestinal Tumors, Liaoning Cancer Hospital & Institute, Cancer Hospital of the Dalian University of Technology
Honjo, Tomoko
Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
Sakaguchi, Yoshihiko
Department of Microbiology, Tokushima Bunri University
Yamauchi, Akira
Department of Biochemistry, Kawasaki Medical School
Kuribayashi, Futoshi
Department of Biochemistry, Kawasaki Medical School
Futami, Junichiro
Department of Interdisciplinary Science and Engineering in Health Systems, Okayama University
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Kondo, Eisaku
Division of Tumor Pathology, Near InfraRed Photo-Immuno-Therapy Research Institute, Kansai Medical University
Inoue, Yusuke
Faculty of Science and Technology, Division of Molecular Science, Gunma University
Toyooka, Shinichi
Department of General Thoracic Surgery and Breast and Endocrinological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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Sakaguchi, Masakiyo
Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
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抄録 | Background Triple-negative breast cancer (TNBC) cells are a highly formidable cancer to treat. Nonetheless, by continued investigation into the molecular biology underlying the complex regulation of TNBC cell activity, vulnerabilities can be exposed as potential therapeutic targets at the molecular level. We previously revealed that lysyl oxidase-like 4 (LOXL4) promotes the invasiveness of TNBC cells via cell surface annexin A2 as a novel binding substrate of LOXL4, which promotes the abundant localization of integrin-beta 1 at the cancer plasma membrane. However, it has yet to be uncovered how the LOXL4-mediated abundance of integrin-beta 1 hastens the invasive outgrowth of TNBC cells at the molecular level.
Methods LOXL4-overexpressing stable clones were established from MDA-MB-231 cells and subjected to molecular analyses, real-time qPCR and zymography to clarify their invasiveness, signal transduction, and matrix metalloprotease (MMP) activity, respectively. Results Our results show that LOXL4 potently promotes the induction of matrix metalloprotease 9 (MMP9) via activation of nuclear factor-kappa B (NF-kappa B). Our molecular analysis revealed that TNF receptor-associated factor 4 (TRAF4) and TGF-beta activated kinase 1 (TAK1) were required for the activation of NF-kappa B through I kappa beta kinase kinase (IKK alpha/beta) phosphorylation. Conclusion Our results demonstrate that the newly identified LOXL4-mediated axis, integrin-beta 1-TRAF4-TAK1-IKK alpha/beta-I kappa beta alpha-NF-kappa B-MMP9, is crucial for TNBC cell invasiveness. |
キーワード | breast cancer
invasion
lysyl oxidase
NF-κB
MMP9
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発行日 | 2024-05-28
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出版物タイトル |
Frontiers in Oncology
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巻 | 14巻
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出版者 | Frontiers Media
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開始ページ | 1371307
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ISSN | 2234-943X
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資料タイプ |
学術雑誌論文
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言語 |
英語
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OAI-PMH Set |
岡山大学
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著作権者 | © 2024 Jiang, Chen, Tomonobu, Kinoshita, Komalasari, Kasano-Camones, Ninomiya, Murata, Yamamoto, Gohara, Ochi, Ruma, Sumardika, Zhou, Honjo, Sakaguchi, Yamauchi, Kuribayashi, Futami, Kondo, Inoue, Toyooka and Sakaguchi.
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論文のバージョン | publisher
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PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.3389/fonc.2024.1371307
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ライセンス | https://creativecommons.org/licenses/by/4.0/
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Citation | Jiang F, Chen Y, Tomonobu N, Kinoshita R, Komalasari NLGY, Kasano-Camones CI, Ninomiya K, Murata H, Yamamoto K-i, Gohara Y, Ochi T, Ruma IMW, Sumardika IW, Zhou J, Honjo T, Sakaguchi Y, Yamauchi A, Kuribayashi F, Futami J, Kondo E, Inoue Y, Toyooka S and Sakaguchi M (2024) Dissection of the signal transduction machinery responsible for the lysyl oxidase-like 4-mediated increase in invasive motility in triple-negative breast cancer cells: mechanistic insight into the integrin-β1-NF-κB-MMP9 axis. Front. Oncol. 14:1371307. doi: 10.3389/fonc.2024.1371307
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助成機関名 |
Japan Society for the Promotion of Science
Zhejiang Provincial Natural Science Foundation of China
National Natural Science Foundation of China
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助成番号 | 23H02748
23K06717
22K20793
23K14595
LQ21H160021
82103072
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