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作 者:吴楠[1] 张文[1] 梁玉龙[1] 靳嘉巍[1] 王丽影[1] 蔡秀梅[1] 查锡良[1]
机构地区:[1]卫生部糖复合物重点实验室-复旦大学上海医学院生物化学与分子生物学系,上海200032
出 处:《复旦学报(医学版)》2006年第2期171-174,182,共5页Fudan University Journal of Medical Sciences
基 金:863基金(2002-BAC11A11)资助
摘 要:目的本研究是利用双向电泳及质谱技术进一步了解全反式视黄酸对人肝癌细胞的作用机制。方法应用双向凝胶电泳技术分离并筛查全反式视黄酸作用后差异表达的蛋白质,并通过质谱技术对差异显著的蛋白质进行鉴定。应用Western blot方法检测7721细胞、肝癌和癌旁组织profilin1蛋白表达水平。结果profi-lin1在SMMC-7721细胞中受全反式视黄酸作用表达上调,这种上调作用对全反式视黄酸具有剂量依赖性,pro-filin1在肝癌组织中较癌旁组织的蛋白表达低。结论profilin1在肝癌组织中表达较癌旁组织低,而全反式视黄酸可诱导肝癌细胞中profilin1表达升高,profilin1可能参与了全反式视黄酸对肿瘤的某些作用过程。Purpose To further illuminate the mechanism responsible for all-trans retinoic acid (atRA) effecting on hepatocarcinoma cells. Methods Using two-dimensional electrophoresis (2-DE), we analyzed differential expressed proteins of atRA-treated and control cells in hepatocellular carcinoma cell line SMMC-7721. Then, we identified the proteins by mass spectrometry (MS) and database searching. Using Western blotting, we detected expression of profilin 1 in 7721 cells, hepatocarcinoma tissues and adjacent noncancerous tissues. Results Profilin 1 expression was lower in hepatocarcinoma tissue than in noncancerous tissue. In SMMC-7721 cells treated with atRA, Profilin 1 was upregulated in a dose-dependent manner. Conclusions Profilin 1 was lower expression in hepatocarcinoma than in noncancerous tissue, and atRA could induced upregulation of profilin 1 which might be involved its effect on hepatocarcinoma.
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