HCVc-SMYD3-RASSF1A途径在肝门部胆管癌发生中的作用
基本信息
结项摘要
丙型肝炎病毒核心蛋白(HCV-C)导致肝门部胆管癌的形成已被认可，但具体机制仍不清楚。研究表明，组蛋白甲基化异常可激活癌基因、细胞周期调控基因，多层次、多途径的参与或促进肿瘤的发生，而DNA甲基化则主要在转录水平抑制抑癌基因的表达，进而影响肿瘤的发生。我们发现：①组蛋白甲基转移酶SMYD3在HCV-C阳性肝门部胆管癌组织中的高表达；②SMYD3能诱导抑癌基因RASSF1A启动子过甲基化、下调其抑癌活性。由此我们提出假设：HCV-C作为病因，从表观遗传学水平，通过SMYD3介导调控RASSF1A抑癌活性，参与肝门部胆管癌的发生。本项目拟着重开展HCV-C对SMYD3表达的调控作用以及SMYD3诱导RASSF1A启动子过甲基化机制等研究，旨在明确组蛋白甲基化在HCV-C致肝门部胆管癌发生的作用，阐明肝门部胆管癌发生的表观遗传学调控机制，为肝门部胆管癌治疗新靶点提供充分的科学依据。
项目摘要
项目成果
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数据更新时间：2023-05-31
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