Continuous taurocholic acid exposure promotes esophageal squamous cell carcinoma progression due to reduced cell loss resulting from enhanced vascular development.

• Material Type: 博士論文
• ISSN: 1932-6203
• Title: Continuous taurocholic acid exposure promotes esophageal squamous cell carcinoma progression due to reduced cell loss resulting from enhanced vascular development.
• Volume: 9 2
• Author/Editor: SATO, Sho
• Author Heading: SATO, Sho
• Publication, Distribution, etc.: PLoS one
• Publication Date: 2014-02-14
• Publication Date (W3CDTF): 2014-02-14
• Periodical title: PLoS one
• Degree grantor/type: 滋賀医科大学
• Date Granted: 2015-09-09
• Date Granted (W3CDTF): 2015-09-09
• Dissertation Number: 乙第419号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 乙第419号
• Text Language Code: eng
• Target Audience: 一般
• Note (General): Background:Refluxogenic effects of smoking and alcohol abuse may be related to the risk of esophageal squamous cell carcinoma (ESCC). The present study attempts to clarify the effects of continuous taurocholic acid (TCA) exposure, which is neither mutagenic nor genotoxic, on ESCC progression.; Methods:A squamous carcinoma cell line (ESCC-DR) was established from a tumor induced in a rat model of gastroduodenal reflux. ESCC-DR cells were incubated with 2 mM TCA for ≥2 months. The effects of continuous TCA exposure were evaluated in vitro on cell morphology, growth, and invasion and in vivo on xenograft tumor growth in nude mice. Moreover, the mean level of secreted transforming growth factor (TGF)-β1 and vascular endothelial growth factor (VEGF) proteins in cell culture supernatants and mRNA synthesis of TGF-β1 and VEGF-A of ESCC cells were measured. The angiogenic potential was further examined by a migration assay using human umbilical vein endothelial cells (HUVECs).; Results:Continuous TCA exposure induced marked formation of filopodia in vitro. Expression levels of angiogenic factors were significantly higher in the cells treated with TCA than in control cells. Tumor xenografts derived from cells pre-exposed to TCA were larger and more vascularized than those derived from control cells. In addition, TCA exposure increased HUVEC migration.; Conclusion:Continuous TCA exposure enhanced ESCC progression due to reduced cell loss in vivo. Cell loss was inhibited by TCA-induced vascular endothelial cell migration, which was mediated by TGF-β1 and VEGF-A released from ESCC cells.; Thesis or Dissertation; 平成27年度; 10.1371/journal.pone.0088831
• DOI: info:doi/10.1371/journal.pone.0088831; https://doi.org/info:doi/10.1371/journal.pone.0088831
• Persistent ID (NDL): info:ndljp/pid/9550899; https://dl.ndl.go.jp/pid/9550899
• 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): 2015-12-01T13:36:39+09:00
• Date Created (W3CDTF): 2017-02-17
• 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/10422/10974; https://shiga-med.repo.nii.ac.jp/records/1378
• 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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