全反式维甲酸对HepG2肝癌干细胞增殖能力的影响

摘要

目的 探讨全反式维甲酸(all-transretinoic acid,ATRA)对HepG2肝癌干细胞增殖能力的影响.方法 选取HepG2肝癌细胞接种于96孔板并培养、鉴定肝癌干细胞,依据随机分配原则分为ATRA组和对照组,每组48孔,ATRA组加入5 μmol/L的ATRA,对照组不作任何处理.结果 Cyclin D、STAT3的蛋白质印迹法灰度值对照组呈逐渐上升趋势,ATRA组先升高后降低,ATRA组的5、7、14 d水平明显低于对照组,差异有统计学意义(P<0. 05);G0/G1期细胞占比对照组无明显变化,ATRA组呈逐渐上升趋势, ATRA组的5、7、14 d水平明显高于对照组,差异有统计学意义(P<0. 05);干细胞A570值对照组呈逐渐上升趋势,ATRA组呈逐渐下降趋势,ATRA组的5、7、14 d水平明显低于对照组,差异有统计学意义(P<0. 05).结论 ATRA可有效抑制HepG2肝癌干细胞的增殖能力,其机制可能与下调干细胞Cyclin D、STAT3等基因蛋白表达水平而阻滞干细胞在G0/G1期细胞周期有关.%Objective To investigate the effect of all-transretinoic acid ( ATRA) on the multiplication capacity of HepG2 hepatocarcinoma stem cells. Methods HepG2 liver cancer cells were inoculated on 96-well plates and hepato-carcinoma stem cells were cultured and identificated, which based on the principles randomly assigned into the ATRA group and control group, each group of 48 hole, ATRA group was given 5 μmol/L ATRA and the control group did not make any processing. Results Expressions of Cyclin D and STAT3 by Western blotting method in the control group showed a trend of rising, those in ATRA group reduced after rising first, expressions of Cyclin D and STAT3 in the 5, 7, 14 days in the ATRA group were significantly lower than those in the control group, the difference was statistically significant (P<0. 05). G0/G1 cell proportion in the control group showed no significant change, that in the ATRA group showed a gradual upward trend, G0/G1 cell proportion in the 5, 7, 14 days in the ATRA group were significantly higher than those in the control group, the difference was statistically significant (P<0. 05). The stem cell A570 value in the control group showed a gradual upward trend, that in the ATRA group showed a gradual decline, the stem cell A570 value in the 5, 7, 14 days in the ATRA group were significantly lower than those in the control group, the differ-ence was statistically significant ( P<0. 05) . Conclusion ATRA can effectively inhibit the proliferation of HepG2 hep-atocarinoma stem cells, and its mechanism may be related to the reduction of gene protein expressions of Cyclin D and STAT3 in stem cells and blocking stem cells in G0/G1 cell cycle.