IL-1αはエナメル上皮腫細胞においてMMP-9の発現を促進し、腫瘍細胞の運動性、局所浸潤性を高める

• 資料種別: 博士論文
• タイトル: IL-1αはエナメル上皮腫細胞においてMMP-9の発現を促進し、腫瘍細胞の運動性、局所浸潤性を高める
• 著者・編者: 小野, 裕右
• 著者標目: 小野, 裕右
• 出版事項: John Wiley & Sons
• 出版年月日等: 2023-07-19
• 出版年（W3CDTF）: 2023-07-19
• 並列タイトル等: Interleukin-1α promotes matrix metalloproteinase-9expression, cellular motility, and local invasiveness ofameloblastoma cells
• 授与機関名: 鹿児島大学
• 授与年月日: 2023-07-19
• 授与年月日（W3CDTF）: 2023-07-19
• 報告番号: 甲総研第708号
• 学位: 博士(歯学)
• 本文の言語コード: eng
• 件名標目: AM-3; ameloblastoma; fibroblast; invasion; macrophage; tumor microenvironment
• 対象利用者: 一般
• 一般注記: 出版タイプ： AM; 博士論文全文, 博士論文要旨, 最終試験結果の要旨, 論文審査の要旨; AimAlthough ameloblastoma is a benign tumor, its local invasiveness and recurrence rate are both high. Thus, the regulation of the invasiveness of ameloblastoma cells into the surrounding tissue is required to understand its pathogenesis. Ameloblastoma cells secrete several matrix metalloproteinases (MMPs); however, the factors inducing their secretion remain unclear. We previously suggested that interleukin (IL)-1α derived from ameloblastoma cells triggers the production of inflammatory cytokines by stromal fibroblasts. In this study, we estimated whether IL-1α affects the behavior of ameloblastoma cells.MethodsThe gene expression of MMP-9 was assessed by real-time reverse transcription–polymerase chain reaction (RT-PCR). The secretion of MMP-9 was assessed by enzyme-linked immunosorbent assay (ELISA). The motility of AM-3 ameloblastoma and Raw264.7 （macrophage derived cells） cells and the invasiveness of AM-3 cells were calculated using the Boyden chamber. The invasiveness of AM-3 cells toward human foreskin fibroblast (HFF)-2 fibroblasts were assessed using modified double-layered collagen gel hemisphere (DL-CGH).ResultsThe mRNA expression and secretion of MMP-9 by AM-3 ameloblastoma cells were significantly increased by IL-1α stimulation. The motilities of AM-3 and RAW264.7 macrophage derived cells and the invasiveness of AM-3 cells were significantly enhanced by IL-1α and suppressed by an IL-1 receptor antagonist (IL-1Ra). The invasiveness of AM-3 cells towards HFF-2 fibroblasts in a DL-CGH model was suppressed by a treatment with IL-1Ra or an anti-IL-1α neutralizing antibody.ConclusionIL-1α itself or the IL-1α-dependent production of unidentified chemo attractants by stromal cells may be important for the local invasiveness of ameloblastoma cells, and IL-1α might be a therapeutic target of the ameloblastoma.; Yusuke Ono, Takao Fuchigami, Michiko Kishida, Hirofumi Koyama, Mikio Iijima, Kazuki Oishi, Toshiro Kibe, Kiyohide Ishihata, Yoshiaki Nishizawa, Tohru Kiyono, Norifumi Nakamura, Shosei KishidaInterleukin-1α promotes matrix metalloproteinase-9 expression, cellular motility, and local invasiveness of ameloblastoma cellsOral Science International 2024;21:112–120.https://doi.org/10.1002/osi2.1193; This is the peer reviewed version of the following article: [ https://onlinelibrary.wiley.com/doi/full/10.1002/osi2.1193 ], which has been published in final form at [ https://doi.org/10.1002/osi2.1193 ]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.
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• コレクション（共通）: 障害者向け資料
• コレクション（障害者向け資料：レベル1）: テキストデータ
• コレクション（個別）: 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• 収集根拠: 博士論文（自動収集）
• 記録形式（IMT）: application/pdf
• オンライン閲覧公開範囲: 国立国会図書館内限定公開
• デジタル化資料送信: 図書館・個人送信対象外
• 遠隔複写可否（NDL）: 可
• 掲載誌（URI）: http://hdl.handle.net/10232/0002000007
• 連携機関・データベース: 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp