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作 者:李潇瑾 徐安健[1] 周东虎 张蓓[1] 黄坚[1] LI Xiao-jin;XU An-jian;ZHOU Dong-hu(Experimental and Translational Research Center,Beijing Friendship Hospital,Capital Medical Universit;Beijing Clinical Medicine Institute,Beijing 100050,China)
机构地区:[1]首都医科大学附属北京友谊医院科研实验中心北京市临床医学研究所,北京100050
出 处:《临床和实验医学杂志》2018年第19期2017-2021,共5页Journal of Clinical and Experimental Medicine
基 金:国家自然科学基金(81602032);北京市优秀人才项目(2016000021469G224);首都医科大学附属北京友谊医院科研启动基金(yyqdkt2015-17)
摘 要:目的探讨肝癌中着丝粒蛋白F(CENPF)的表达量与细胞增殖、迁移等生物学行为的关系及其作用机制。方法比较肝癌细胞与正常肝细胞、肝癌组织与癌旁正常组织中CENPF的表达量。利用慢病毒包被的质粒转染肝癌细胞干扰CENPF的表达,分别使用MTS试剂、台盼兰染色法、transwell迁移小室方法研究CENPF的表达对细胞增殖、存活、迁移的影响,并利用Western blotting法探究其对细胞周期调控蛋白c-Myc、Cyclin D1表达的影响,明确CENPF作用机制。结果与正常肝细胞和癌旁正常组织相比,肝癌细胞和肝癌组织中CENPF蛋白表达量显著增加。使用病毒包被的质粒抑制CENPF的表达可显著降低肝癌细胞的增殖能力、存活率和迁移能力,同时调控细胞增殖和细胞周期的蛋白(c-Myc、Cyclin D1)的表达降低。结论肝癌中过表达的CENPF可通过激活细胞周期调控蛋白c-Myc和Cyclin D1,提高肝癌细胞的增殖、存活、迁移能力,诱导肝癌的发生和发展。Objective To explore the association between CENPF expression and the cell biological behavior, such as cell proliferation and migration in hepatocellular carcinoma. Methods The expression of CENPF in hepatocellular carcinoma cells, normal liver cells, hepatocellular carcinoma tissue and paracancerous tissue were detected by qRT-PCR and Western blot. The effects of CENPF expression on cell proliferation, survival, migration and the expression of cell cycle regulatory proteins c-Myc and Cyclin D1 were studied by MTS, trypan blue staining, transwell chamber and Western blot using lentivirus packaged plasmid interference. Results Compared with normal liver cells and paracancerous tissue, the expression of CENPF in hepatocellular carcinoma cell lines and tissue were significantly higher. The proliferation rate, survival rate, migration rate, and the expression of cell proliferation and cycle regulatory protein (c-Myc and Cyclin D1) in hepatocellular carcinoma cells were decreased by inhibiting CENPF expression. Conclusion Overexpression of CENPF in hepatocellular carcinoma promoted cell proliferation, survival, and migration by activating cell cycle regulation protein c-Myc and Cyclin D1, thus inducing hepatocellular carcinoma and its development.
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