Extracellular vesicle-encapsulated miR-30e suppresses cholangiocarcinoma cell invasion and migration via inhibiting epithelial-mesenchymal transition

• Material Type: 博士論文
• ISSN: 1949-2553
• Title: Extracellular vesicle-encapsulated miR-30e suppresses cholangiocarcinoma cell invasion and migration via inhibiting epithelial-mesenchymal transition
• Volume: 9 23
• Author/Editor: 太田, 雄
• Publication Date: 2018-03
• Publication Date (W3CDTF): 2018-03
• Alternative Title: Mir-30eは細胞外小胞EVによる細胞間伝達を介し上皮間葉形質転換EMTの抑制を経て胆管癌細胞の浸潤・遊走能を阻害する
• Periodical title: Oncotarget
• Degree grantor/type: 旭川医科大学
• Date Granted: 2019-03-25
• Date Granted (W3CDTF): 2019-03-25
• Dissertation Number: 甲第532号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第532号
• Text Language Code: eng
• Subject Heading: cholangiocarcinoma; epithelial-mesenchymal transition (EMT); exosome; extracellular vesicles; microRNA (miRNA)
• Note (General): Early-staged cholangiocarcinoma (CCA) is difficult to diagnose due to its high potential for invasion and metastasis. Epithelial-mesenchymal transition (EMT) is induced by transforming growth factor-β (TGF-β) in a process thought to be important for invasion and metastasis in several cancers, including CCA. Although microRNAs (miRNAs) have been implicated in the pathogenesis of several malignancies, their roles to CCA are not clearly understood. Some miRNAs were reported to be included in extracellular vesicles (EVs) and transferred from their donor cells to other cells, modulating recipient cell behaviors. In this study, the involvement and functional roles of EV-contained miRNAs during EMT in human CCA were determined. Expression profiling identified a subset of miRNAs that were reduced by TGF-β in CCA cells. Among these, miR-30e was highly downregulated by TGF-β and predicted to target Snail, which is an EMT-inducible transcription factor. MiR-30e overexpression suppressed cell invasion and migration via inhibiting EMT, whereas miR-30e inhibition promoted EMT, cell invasion and migration. Moreover, miR-30e was enriched in EVs derived from CCA cells after miR-30e overexpression, and miR-30e intercellular transfer through EVs suppressed EMT, cell invasion and migration in recipient CCA cells. Together, our results suggest that EV-mediated miR-30e transfer could inhibit EMT via directly targeting Snail, which subsequently suppresses CCA cell invasion and migration. These findings provide several new insights into regulatory mechanisms of tumor invasion and metastasis in human CCA.; identifier:PMID：29662654; 開始ページ : 16400; 終了ページ : 16417
• DOI: info:doi/10.18632/oncotarget.24711; https://doi.org/info:doi/10.18632/oncotarget.24711
• Persistent ID (NDL): info:ndljp/pid/11278856; https://dl.ndl.go.jp/pid/11278856
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 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
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2019-05-06T10:27:56+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
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• Periodical Title (URI): http://amcor.asahikawa-med.ac.jp/modules/xoonips/detail.php?id=20190325_K532
• Data Provider (Database): 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