维甲酸对肝癌细胞HepG2糖基化磷脂酰肌醇特异性磷酯酶D表达及细胞生物学特性的影响

摘要

应用MTT、流式细胞仪、免疫印迹法检测全反式维甲酸(ATRA)单独或联合糖基化磷脂酰肌醇特异性磷酯酶D (GPI-PLD)特异性抑制剂1,10-二氮杂菲对肝癌细胞HepG2生物学特性的改变.ATRA使肝癌细胞HepG2 GPI-PLD基因表达及酶活性上调,并呈现剂量和时间依赖性.ATRA可抑制肝癌细胞HepG2增殖,使肝癌细胞Caspase-3表达水平显著增加,Bcl-2表达水平下调,促进肝癌细胞凋亡(P＜0.05).ATRA联合1,10-二氮杂菲诱导组细胞,Bcl-2、细胞增殖活性较ATRA单独诱导组显著增强,Caspase-3、凋亡率显著下降.维甲酸可促进肝癌细胞HepG2 GPI-PLD基因表达上调,高活性的GPI-PLD有助于维甲酸抑制肝癌细胞增殖,促进肝癌细胞凋亡.%The biological characteristics change of HepG2 cells, induced by all-trans retinoic acid (ATRA) alone or combination with glycosylphosphatidylinositol specific phospholipase D (GPI-PLD) specific inhibitor 1, 10-phenanthroline, were detected by MTT, flow cytometry and Western blot. The hepatoma cells HepG2 GPI-PLD gene expression was upregulated by ATRA in a dose and time dependent. ATRA inhibited the proliferation of HepG2 cells, decreased the Bcl-2 expression levels, increased the Caspase 3 expression levels and promoted hepatocellular apoptosis significantly(P<0.05). Compared to ATRA alone, the Bcl-2 expression levels, cell proliferation activity of the HepG2 cells induced by ATRA combined 1, 10-phenanthroline were significantly increased, and the caspase-3 expression levels, apoptosis was significantly decreased. A-TRA can promote GPI-PLD gene expression in hepatoma cell HepG2 and high activity of GPI-PLD help to prevent cell proliferation and promote apoptosis of hepatoma cells induced by ATRA.