Inhibition of Heparanase Expression Results in Suppression of Invasion, Migration and Adhesion Abilities of Bladder Cancer Cells. 11

• Material Type: 博士論文
• ISSN: 1422-0067
• Title: Inhibition of Heparanase Expression Results in Suppression of Invasion, Migration and Adhesion Abilities of Bladder Cancer Cells.
• Volume: 21 11
• Author/Editor: Tatsumi, Yoshihiro; Miyake, Makito; Shimada, Keiji; Fujii, Tomomi; Hori, Shunta; Morizawa, Yosuke; Nakai, Yasushi; Anai, Satoshi; Tanaka, Nobumichi; Konishi, Noboru; Fujimoto, Kiyohide
• Author Heading: Tatsumi, Yoshihiro; Miyake, Makito; Shimada, Keiji; Fujii, Tomomi; Hori, Shunta; Morizawa, Yosuke; Nakai, Yasushi; Anai, Satoshi; Tanaka, Nobumichi; Konishi, Noboru; Fujimoto, Kiyohide
• Publication, Distribution, etc.: MDPI
• Publication Date: 2020-05-27; 21 11
• Publication Date (W3CDTF): 2020-05-27
• Alternative Title: 膀胱癌細胞株において、ヘパラナーゼを阻害することにより、細胞浸潤、遊走、接着能を抑制する
• Periodical title: International journal of molecular sciences
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2021-03-15
• Date Granted (W3CDTF): 2021-03-15
• Dissertation Number: 乙第1506号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 乙第1506号
• Text Language Code: eng
• Subject Heading: heparanase; syndecan-1; heparan sulfate proteoglycans (HSPGs); urothelial carcinoma
• Target Audience: 一般
• Note (General): type:Thesis; Heparan sulfate proteoglycan syndecan-1, CD138, is known to be associated with cell proliferation, adhesion, and migration in malignancies. We previously reported that syndecan-1 (CD138) may contribute to urothelial carcinoma cell survival and progression. We investigated the role of heparanase, an enzyme activated by syndecan-1 in human urothelial carcinoma. Using human urothelial cancer cell lines, MGH-U3 and T24, heparanase expression was reduced with siRNA and RK-682, a heparanase inhibitor, to examine changes in cell proliferation activity, induction of apoptosis, invasion ability of cells, and its relationship to autophagy. A bladder cancer development mouse model was treated with RK-682 and the bladder tissues were examined using immunohistochemical analysis for Ki-67, E-cadherin, LC3, and CD31 expressions. Heparanase inhibition suppressed cellular growth by approximately 40% and induced apoptosis. The heparanase inhibitor decreased cell activity in a concentration-dependent manner and suppressed invasion ability by 40%. Inhibition of heparanase was found to suppress autophagy. In N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer mice, treatment with heparanase inhibitor suppressed the progression of cancer by 40%, compared to controls. Immunohistochemistry analysis showed that heparanase inhibitor suppressed cell growth, and autophagy. In conclusion, heparanase suppresses apoptosis and promotes invasion and autophagy in urothelial cancer.; 博士（医学）・乙第1506号・令和3年3月15日; © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open accessarticle distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license (http://creativecommons.org/licenses/by/4.0/).; identifier:International journal of molecular sciences Vol.21 No.11 Article No.3789 (2020 May); identifier:14220067; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/3932; identifier:International journal of molecular sciences, 21(11): Article No.3789
• DOI: info:doi/10.3390/ijms21113789; https://doi.org/info:doi/10.3390/ijms21113789
• Persistent ID (NDL): info:ndljp/pid/12154394; https://dl.ndl.go.jp/pid/12154394
• 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): 2022-03-06T04:54:00+09:00
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/10564/3932
• 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

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