Effects of galectin-9 on apoptosis, cell cycle and autophagy in human esophageal adenocarcinoma cells

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DOI[info:doi/10.3892/or.2017.5689]to the data of the same series

Effects of galectin-9 on apoptosis, cell cycle and autophagy in human esophageal adenocarcinoma cells

Persistent ID (NDL): info:ndljp/pid/11122663

Material type: 博士論文

Author: 明石, 瑛美子

Publisher: -

Publication date: 2018-03-24

Material Format: Digital

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Name of awarding university/degree: 香川大学,博士（医学）

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Note (General)：: AbstractThe incidence of esophageal adenocarcinoma (EAC) is rapidly increasing in western countries. The overall mortality of this disease remains hig...

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Material Type: 博士論文
Title: Effects of galectin-9 on apoptosis, cell cycle and autophagy in human esophageal adenocarcinoma cells
Author/Editor: 明石, 瑛美子
Author Heading: 明石, 瑛美子
Publication Date: 2018-03-24
Publication Date (W3CDTF): 2018-03-24
Degree grantor/type: 香川大学
Date Granted: 2018-03-24
Date Granted (W3CDTF): 2018-03-24
Dissertation Number: 甲第687号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第687号
Text Language Code: eng
Alias of Author: Akashi, Emiko
Subject Heading: esophageal adenocarcinoma
galectin-9
apoptosis
microRNAs
angiogenesis
Target Audience: 一般
Note (General): AbstractThe incidence of esophageal adenocarcinoma (EAC) is rapidly increasing in western countries. The overall mortality of this disease remains high with a 5-year survival rate of less than 20%, despite remarkable advances in the care of patients with EAC. Galectin-9 (Gal-9) is a tandem-repeat type galectin that exerts anti-proliferative effects on various cancer cell types. The aim of the present study was to evaluate the effects of Gal-9 on human EAC cells and to assess the expression of microRNAs (miRNAs) associated with the antitumor effects of Gal-9 in vitro. Gal-9 suppressed the proliferation of the EAC cell lines OE19, OE33, SK-GT4, and OACM 5.1C. Additionally, Gal-9 treatment induced apoptosis and increased the expression levels of caspase-cleaved cytokeratin 18, activated caspase-3 and activated caspase-9. However, it did not promote cell cycle arrest by reducing cell cycle-related protein levels. Furthermore, Gal-9 increased the level of the angiogenesis-related protein interleukin-8 (IL-8) and markedly altered miRNA expression. Based on these findings, Gal-9 may be of clinical use for the treatment of EAC.
DOI: info:doi/10.3892/or.2017.5689
https://doi.org/info:doi/10.3892/or.2017.5689
Persistent ID (NDL): info:ndljp/pid/11122663
https://dl.ndl.go.jp/pid/11122663
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): 2018-08-03T23:36:01+09:00
Date Created (W3CDTF): 2020-10-27
Format (IMT): 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): https://kagawa-u.repo.nii.ac.jp/records/307
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