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      1. 當前位置:首頁 > 智慧健康列表 > 腦科學和醫療技術 > 詳細信息
        前列腺素PGE2 對肝癌細胞CD29 表達調控及相關機制的研究
        來源: | 作者: | 發布時間:2014-4-15 14:49:10

        前列腺素PGE2 對肝癌細胞CD29 表達調控及相關機制的研究
        王潔,白小明,冷靜
        基金項目:高等學校博士學科點專項科研基金資助(20113234120009)
        作者簡介:王潔(1986),女,研究生,主要研究方向:PGE2 對肝癌細胞侵襲能力的影響
        通信聯系人:冷靜(1954),男,教授,主要研究方向:PGE2 對腫瘤細胞生長與擴散的影響及其機制.

         (南京醫科大學病理學系,南京 210029)
        摘要:目的:闡明前列腺素E2(prostaglandin E2, PGE2)通過EP1 受體上調肝癌細胞Huh-7 中CD29 的表達及其相關的信號轉導通路。方法:用PGE2、EP1 受體激動劑(17-phenyltrinor Prostaglandin E2,17-PT-PGE2)、EP1 受體抑制劑SC19220、NF-κB 抑制劑PDTC 處理Huh-7 細胞,通過Western blot、免疫熒光實驗等方法檢測CD29 蛋白表達水平和NF-κB 的活性。結果:5μmol/L 的PGE2 處理Huh-7 細胞24h 后,CD29 的表達水平與對照組相比上升了129.48% (P<0.01),5μmol/L EP1 受體激動劑17-PT-PGE2 處理后使細胞CD29 的蛋白表達水平升高了216.34%(P<0.01)。10μmol/L 的EP1 受體抑制劑SC19220 處理后CD29 表達水平與PGE2 組相比下降了79.19%(P<0.05)。免疫熒光實驗顯示17-PT-PGE2 處理Huh-7 細胞120min 后,NF-κB 核表達水平明顯增加;Western blot 實驗顯示Phospho-NF-κB-P65 水平明顯增高。NF-κB 抑制劑PDTC 處理Huh-7 細胞后CD29 蛋白表達水平與EP1 受體激動劑組相比降低了94.95%(P<0.01)。結論:PGE2 可通過EP1 受體上調Huh-7 細胞中CD29 的表達,此調節作用可能與NF-κB 信號轉導通路有關。
        關鍵詞:病理學;前列腺素E2;EP1 受體;CD29;NF-κB
        中圖分類號:R735.7

        The role of PGE2 on CD29 expression and its related mechanism in hepatocellular carcinoma
        WANG Jie, BAI Xiaoming, LENG Jing
        (Department of Pathology, Nanjing Medical University, Nanjing 210029)
        Abstract: Objective: To investigate the effect of prostaglandin E2 (PGE2) on the expression of CD29 and its related signaling pathway by EP1 receptor in Huh-7 cells. Methods: Huh-7 cells were treated with PGE2, EP1 receptor agonist(17-phenyltrinor Prostaglandin E2), EP1 receptor antagonist SC19220,NF-κB inhibitor PDTC,Western blot and immunofluorescence test
        were employed to detect the expression of CD29 and activation of NF-κB in Huh-7 cells.Results:The level of CD29 was increased by 129.48%(P<0.01) after being treated with 5μmol/L PGE2 for 24h, The level of CD29 was increased by 216.34%(P<0.01)after being treated with EP1 receptor agonist (5μmol/L ) for 24h. the expression level of CD29 was decreased by 79.19%(P<0.05) after being treated with EP1 receptor antagonist SC19220 (10μmol/L). The expression lever of cell nucleus was obviously increased for 120min by immunofluorescence; The level of 35 Phospho-NF-κB-P65 was increased through Western blot. After the treatment of NF-κB inhibitor PDTC , the level of CD29 was decreased by 94.95% (P<0.01). Conclusion: PGE2 might up-regulate the expression level of CD29 through EP1 receptor in Huh-7 cells, which could be partly related to the NF-κB signaling pathway.
        Key words: Pathology; PGE2; EP1 receptor; CD29; NF-κB

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