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2β(3羟丙氧基)骨化三醇对人肝癌细胞周期阻滞及P^(27kip1)蛋白的诱导表达

Effects of 2β-(3-hydroxyproxy)-calcitriol on differentiation of human liver carcinoma cell line and induction of P^(27kip1)
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摘要 目的探讨2β(3羟丙氧基)骨化三醇(ED-71)诱导人肝癌细胞HepG2生长抑制和细胞周期G1阻滞,及对抑癌基因P27kip1表达的影响。方法培养HepG2,应用四甲基偶氮唑盐(MTT)比色法观察ED-71对HepG2的生长抑制作用,流式细胞术分析细胞周期,以Western-blot检测HepG2细胞中P27kip1蛋白的表达水平。结果ED-71处理后HepG2的生长缓慢,细胞生长受到明显抑制。细胞阻滞于G1期(80.6±2.6,48.7±3.0,P<0.05),P27kip1蛋白表达水平增强(0.11±0.06,0.67±0.08,P<0.05)。结论ED-71抑制人肝癌细胞株HepG2的生长,诱导人肝癌细胞分化,使细胞阻滞于G1期,可能与ED-71诱导人肝癌细胞中抑癌基因P27kip1蛋白的表达有关。 Purpose To explore the effects of 2β-（3-hydroxyproxy）-calcitriol（ED-71 ） on proliferation, differentiation, phase growth arrest and induction of P^27kip1 in human liver carcinoma cell line HepG2. Methods Carcinoma cells HepG2 was treated with ED-71 at different concentrations. MTT assay was adopted to describe the proliferation of carcinoma cells. Light microscopy was used to find morphological changes in carcinoma cells. Cell cycle was determined by flow cytometry. Expression of P^27kip1 Was determined by Western-blot. The statistical analysis was performed using one-way ANOVA and student t test. Results ED-71 treatment led to a time-and dose-dependent inhibition in carcinoma cells HepG2 proliferation. ED-71 treatment caused a decline in the fraction of S-phase cells and an increase in G0/G1 eells.ED-71 improved the expression of P^27kip1. Conclusion ED-71 treatment could inhibit proliferation of human liver carcinoma cell HepG2 ,cause partial differentiation and induce the expression of P^27kip1.
作者 刘东兴 孟玫 朱菊人 秦成勇
机构地区 山东大学山东省立医院
出处 《中国生化药物杂志》 CAS CSCD 2007年第1期43-45,共3页 Chinese Journal of Biochemical Pharmaceutics
关键词 2β(3羟丙氧基)骨化三醇 细胞周期 抑癌基因 P^27kip1 2β- （3-hydroxyproxy）-calcitriol （ ED-71 ） cell cycle antioncogene P^27kip1
分类号 R979.1 [医药卫生—药品] R965 [医药卫生—药理学]
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参考文献11

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共引文献12

中国生化药物杂志
2007年 第1期

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