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作 者:梁琳慧[1] 吴顺泉[1] 应巧[1] 丁洁[1] 黄胜林[1] 姚坚[1] 何祥火[1]
机构地区:[1]上海市肿瘤研究所癌基因及相关基因国家重点实验室,上海200032
出 处:《胃肠病学和肝病学杂志》2009年第12期1095-1098,共4页Chinese Journal of Gastroenterology and Hepatology
基 金:上海市卫生局科技发展基金(2007088);上海市科委"创新行动计划"重大基础研究项目(07DJ14006)
摘 要:目的研究CPGL-B抑制肝癌增殖的分子机制。方法将CPGL-B克隆入慢病毒载体,转染293T细胞包装病毒。之后感染肝癌细胞系,通过CCK-8染色和克隆形成的方法检测细胞增殖的变化,用PI染色的方法检测细胞周期的变化;用western印迹方法检测p21的表达。结果CPGL-B可抑制肝癌细胞的增殖和克隆形成能力,并使细胞阻滞在G1期,上调p21的蛋白水平。结论CPGL-B能够抑制肝癌的增殖,抑制肝癌细胞从G1到S期的转化,这种作用可能是通过上调p21介导的。Objective To investigate the role and mechanism of CPGL-B in inhibiting the proliferation of hepatocel- lular carcinoma. Methods CPGL-B was cloned into the lenti-virus expression vector and transfected into 293T cells. Then SMMC-7721 cells were infected by the produced virus. SMMC-7721 cell growth was determined by CCK-8 assays and colony formation analysis. The cell cycle was analyzed by FACS with PI staining. The expression of p21 was determined by western blot. Results CPGL-B inhibited the cell proliferation of SMMC-7721 and blocked cell cycle at the transition from G1 to S phase. Moreover, CPGL-B could upregulate the protein level of cell cycle inhibitor p21. Conclusion The results show the inhibitory role of CPGL-B in hepatocellular carcinoma cell proliferation and cell cycle progression, and provide the potential mechanism CPGL-B negatively regulated cell growth of hepatocellular carcinoma.
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