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By comparing PDAC to hepatocellular carcinoma (HCC), which is well vascularized, we investigated the mechanisms and tumor biological significance of the poor neovascularization in PDAC. Methods: Surgical specimens from primary PDAC and HCC patients were immunohistologically stained to detect the expressions of CD105, CD44, HIF-1α, PHD3, and Siah2. We also used two PDAC and two HCC cell lines to compare the expressions of HIF-1α, PHD3, and CD44, as well as the production of VEGF in hypoxic condition. The role of PHD3 in regulating HIF-1α expression was further confirmed by siRNA knockdown in a PDAC cell line that highly expressed PHD3. Results: There were significantly fewer microvessels but more cancer stem cells in PDAC specimens compared to HCC specimens. The expression of CD105 was reversely related to the expression of CD44 in PDAC and HCC specimens. PDAC specimens also showed higher expressions of PHD3 but lower expressions of HIF-1α. 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Increased expression of PHD3 represses the HIF-1 signaling pathway and contributes to poor neovascularization in pancreatic ductal adenocarcinoma
http://hdl.handle.net/10069/35876
http://hdl.handle.net/10069/358764750bce7-c091-473c-9d98-b52fcd8e695d
名前 / ファイル | ライセンス | アクション |
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JouGas50_975.pdf (2.3 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2015-10-02 | |||||
タイトル | ||||||
タイトル | Increased expression of PHD3 represses the HIF-1 signaling pathway and contributes to poor neovascularization in pancreatic ductal adenocarcinoma | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | CD44 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | HIF-1α | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | Pancreatic ductal adenocarcinoma | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | PDH3 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | VEGF | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Tanaka, Takayuki
× Tanaka, Takayuki× Li, Tao-Sheng× Urata, Yoshishige× Goto, Shinji× Ono, Yusuke× Kawakatsu, Miho× Matsushima, Hajime× Hirabaru, Masataka× Adachi, Tomohiko× Kitasato, Amane× Takatsuki, Mitsuhisa× Kuroki, Tamotsu× Eguchi, Susumu |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background: Pancreatic ductal adenocarcinoma (PDAC) is known as one of the most malignant potential diseases with poor neovascularization. By comparing PDAC to hepatocellular carcinoma (HCC), which is well vascularized, we investigated the mechanisms and tumor biological significance of the poor neovascularization in PDAC. Methods: Surgical specimens from primary PDAC and HCC patients were immunohistologically stained to detect the expressions of CD105, CD44, HIF-1α, PHD3, and Siah2. We also used two PDAC and two HCC cell lines to compare the expressions of HIF-1α, PHD3, and CD44, as well as the production of VEGF in hypoxic condition. The role of PHD3 in regulating HIF-1α expression was further confirmed by siRNA knockdown in a PDAC cell line that highly expressed PHD3. Results: There were significantly fewer microvessels but more cancer stem cells in PDAC specimens compared to HCC specimens. The expression of CD105 was reversely related to the expression of CD44 in PDAC and HCC specimens. PDAC specimens also showed higher expressions of PHD3 but lower expressions of HIF-1α. Similarly, the expression of PHD3 was observed clearly in PDAC cell lines, but was almost completely negative in HCC cell lines. Hypoxic stimulation clearly enhanced HIF-1α expression and VEGF secretion in both HCC cell lines, but did not significantly change in PDAC cell lines. The knockdown of PHD3 in PDAC cells restored the hypoxic-induced HIF-1α expression, which accordingly stimulated the cells’ VEGF secretion. Conclusions: The enhanced expression of PHD3 might likely contribute to the poor neovascularization and affect the biological characterization in PDAC cancer cells. | |||||
書誌情報 |
Journal of Gastroenterology 巻 50, 号 9, p. 975-983, 発行日 2015-09 |
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出版者 | ||||||
出版者 | 日本消化器病学会 | |||||
出版者別言語 | ||||||
Japanese Society of Gastroenterology | ||||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 09441174 | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 14355922 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1007/s00535-014-1030-3 | |||||
権利 | ||||||
権利情報 | c The Author(s) 2014. This article is published with open access at Springerlink.com | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Journal of Gastroenterology, 50(9), pp.975-983; 2015 |