MicroRNA profiles during galectin-9-induced apoptosis of pancreatic cancer cells

• Material Type: 博士論文
• Title: MicroRNA profiles during galectin-9-induced apoptosis of pancreatic cancer cells
• Author/Editor: 大倉, 亮一
• Author Heading: 大倉, 亮一
• Publication Date: 2016-06-28
• Publication Date (W3CDTF): 2016-06-28
• Degree grantor/type: 香川大学
• Date Granted: 2016-06-28
• Date Granted (W3CDTF): 2016-06-28
• Dissertation Number: 甲第641号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第641号
• Text Language Code: eng
• Alias of Author: Okura, Ryoichi
• Subject Heading: apoptosis; caspase-cleaved keratin 18; cell cycle; cytochrome c; galectin-9; microRNAs; pancreatic cancer
• Target Audience: 一般
• Note (General): AbstractPancreatic cancer is the eighth‑leading cause of cancer‑associated mortality in males and the ninth‑leading cause in females worldwide. Even when diagnosed early enough to be potentially resectable, the prognosis of invasive pancreatic cancer is poor. Galectin‑9 (Gal‑9) is a tandem‑repeat type galectin that has recently been demonstrated to possess an anti‑proliferative effect on cancer cells. Therefore, the present study evaluated the effects of Gal‑9 on the proliferation of human pancreatic cancer cells and examined the microRNAs that are associated with the antitumor effects of Gal‑9. Gal‑9 suppressed the proliferation of multiple pancreatic cancer cell lines. In addition, Gal‑9 treatment increased the levels of caspase‑cleaved keratin 18 and the expression of cytochrome c in pancreatic cancer cell lines. This data suggests that Gal‑9 induces intrinsic apoptosis in pancreatic cancer cell lines through the caspase‑dependent and caspase‑independent pathways. In addition, Gal‑9 reduced the expression levels of phosphorylated epidermal growth factor receptor and numerous receptor tyrosine kinases (RTKs). In conclusion, Gal‑9 may suppress the growth of human pancreatic cancer cells in vitro. These findings suggest that Gal‑9 may be a new therapeutic agent for the treatment of pancreatic cancer.
• DOI: info:doi/10.3892/ol.2017.7316; https://doi.org/info:doi/10.3892/ol.2017.7316
• Persistent ID (NDL): info:ndljp/pid/10952259; https://dl.ndl.go.jp/pid/10952259
• 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): 2017-09-02T15:28:24+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/266
• 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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2019-09-04 再収集