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作 者:刘礼 袁昌劲[1] 郭敬杰 余涛[1] 吕秀玮 刘娇萍 赖晓晶[2]
机构地区:[1]华中科技大学同济医学院附属武汉市中心医院,湖北武汉430012 [2]武汉生物工程学院药学院
出 处:《实用预防医学》2018年第2期160-161,248,共3页Practical Preventive Medicine
基 金:国家自然科学基金(31500840)
摘 要:目的研究5-氮杂胞苷对SGC7901胃癌细胞DKK3基因启动子去甲基化对细胞增殖及凋亡的影响。方法采用5-氮杂胞苷处理SGC7901胃癌细胞,以未行5-氮杂胞苷处理的SGC7901胃癌细胞为对照,比较DKK3基因启动子甲基化改变及细胞增殖曲线、细胞增殖及凋亡的差异。结果 SGC7901胃癌细胞DKK3基因启动子在5-氮杂胞苷作用前呈甲基化状态,作用后呈未甲基化状态,表明5-氮杂胞苷对SGC7901胃癌细胞DKK3基因启动子具有去甲基化作用。5-氮杂胞苷作用后的SGC7901胃癌细胞G_0/G_1期比例、PI和凋亡率均显著高于作用前SGC7901胃癌细胞(均P<0.05),S期和G_2/M期显著低于作用前SGC7901胃癌细胞(均P<0.05)。结论 DKK3基因可能具有抑癌基因作用,5-氮杂胞苷对SGC7901胃癌细胞DKK3基因启动子的去甲基化可促进细胞凋亡并抑制其增殖。Objective To study the 5-azacytidine' s demethylation for dickkopf-related protein 3 ( DKK3) gene and its effects on SGC7901 gastric cancer cells' proliferation and apoptosis. Methods SGC7901 gastric cancer cells were treated with 5-aza- cytidine, and other SGC7901 gastric cancer cells without 5-azacytidine treatment served as the controls. The changes of DKK3 gene promoter' s methylation and the differences in cell proliferation curve, cell proliferation and apoptosis were compared. Results DKK3 gene in SGC7901 gastric cancer cells showed methylation before 5-azacytidine treatment, but showed unmethylation after 5 -azacytidine treatment, indicating that 5-azacytidine induced DKK3 gene promoter's demethylation. The proportion of G0/Gt phase, proliferation index {PI) and apoptosis rate in SGC7901 gastric cancer cells after 5-azaeytidine treatment were all signifi- cantly higher than those in SGC7901 gastric cancer ceils before 5-azaeytidine treatment { all P〈0.05 } , whereas the S-phase and G2/M phase in SGC7901 gastric cancer cells after 5-azacytidine treatment were both significantly lower than those in SGC7901 gas- tric cancer ceils before 5-azacytidine treatment ( both P〈0.05 ). Coneluslons DKK3 may be an anti-oncogene. 5-azacytidine can demethylate DKK3 gene promoter's methylation, which can promote SGC7901 gastric cancer cells' apoptosis and inhibit their proliferation.
关 键 词:5-氮杂胞苷 SGC7901胃癌细胞 DKK3 去甲基化 细胞增殖
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