Galectin-9 suppresses cholangiocarcinoma cell proliferation by inducing apoptosis but not cell cycle arrest

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DOI[info:doi/10.3892/or.2015.4197]to the data of the same series

Galectin-9 suppresses cholangiocarcinoma cell proliferation by inducing apoptosis but not cell cycle arrest

Persistent ID (NDL): info:ndljp/pid/11337522

Material type: 博士論文

Author: 小林, 聖幸

Publisher: -

Publication date: 2015-09-29

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)：: AbstractCholangiocarcinoma is the most common biliary malignancy and the second most common hepatic malignancy after hepatocellular carcinoma (HCC). G...

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Material Type: 博士論文
Title: Galectin-9 suppresses cholangiocarcinoma cell proliferation by inducing apoptosis but not cell cycle arrest
Author/Editor: 小林, 聖幸
Author Heading: 小林, 聖幸
Publication Date: 2015-09-29
Publication Date (W3CDTF): 2015-09-29
Degree grantor/type: 香川大学
Date Granted: 2015-09-29
Date Granted (W3CDTF): 2015-09-29
Dissertation Number: 甲第616号
Degree Type: 博士（医学）
Conferring No. (Dissertation): 甲第616号
Text Language Code: eng
Alias of Author: Kobayashi, Kiyoyuki
Subject Heading: cholangiocarcinoma
galectin-9
apoptosis
cell cycle
microRNAs
cytochromec
epidermal growth factor receptor
angio-genesis
Target Audience: 一般
Note (General): AbstractCholangiocarcinoma is the most common biliary malignancy and the second most common hepatic malignancy after hepatocellular carcinoma (HCC). Galectin-9 (Gal-9) is a tandem-repeat-type galectin that has recently been shown to exert antiproliferative effects on cancer cells. Therefore, the present study evaluated the effects of Gal-9 on the proliferation of human cholangiocarcinoma cells in vitro as well as the microRNAs (miRNAs) associated with the antitumor effects of Gal-9. Gal-9 suppressed the proliferation of cholangiocarcinoma cell lines in vitro and the growth of human cholangiocarcinoma cell xenografts in nude mice. Our data further revealed that Gal-9 increased caspase‑cleaved keratin 18 (CCK18) levels, and the expression of cytochrome c increased in Gal-9-treated cholangiocarcinoma cell lines. These data suggested that Gal-9 induced cholangiocarcinoma cell apoptosis via the intrinsic apoptosis pathway mediated by caspase-dependent or -independent pathways. In addition, Gal-9 reduced the phosphorylation of the epidermal growth factor receptor (EGFR), insulin-like growth factor and insulin-like growth factor-1 receptor (IGF-1R), hepatocyte growth factor receptor and fibroblast growth factor receptor 3 (FGFR3). These findings suggest that Gal-9 can be a candidate of therapeutic target in the treatment of cholangiocarcinoma.
DOI: info:doi/10.3892/or.2015.4197
https://doi.org/info:doi/10.3892/or.2015.4197
Persistent ID (NDL): info:ndljp/pid/11337522
https://dl.ndl.go.jp/pid/11337522
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): 2019-08-03T12:23:27+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/370
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