[1]孙小锦,马琳艳,张梦晓,等.氯喹通过miR-26b调控Mcl-1诱导人肝癌HepG2细胞凋亡[J].南方医科大学学报,2018,(04):409.
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氯喹通过miR-26b调控Mcl-1诱导人肝癌HepG2细胞凋亡()
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《南方医科大学学报》[ISSN:1673-4254/CN:44-1627/R]

卷:
期数:
2018年04期
页码:
409
栏目:
出版日期:
2018-04-30

文章信息/Info

Title:
Chloroquine induces apoptosis of human hepatocellular carcinoma cells in vitro by miR-26b-mediated regulation of Mcl-1
作者:
孙小锦马琳艳张梦晓王颖张配蒋琛琛刘浩
关键词:
肝癌细胞氯喹miR-26bMcl-1凋亡
Keywords:
hepatocellular carcinoma cells chloroquine miR-26b Mcl-1 apoptosis
摘要:
目的探讨氯喹对人肝癌HepG2细胞凋亡的作用及其可能机制。方法选择浓度10、20、40、80、160 μmol/L的氯喹处理细 胞,MTT法检测氯喹对HepG2细胞的增殖抑制作用。试剂盒检测胞内ATP水平,PI单染检测细胞凋亡情况,此外,使用PCR检 测miR-26b水平,Western blot检测Mcl-1蛋白的表达。结果氯喹在10~160 μmol/L浓度范围内对HepG2细胞具有显著的增殖 抑制作用,在80 μmol/L氯喹的作用下24、48、72 h的存活率分别为(71.59±0.2)%、(45.40±0.5)%、(26.34±1.4)%,随浓度增加抑 制率也逐渐增加。同时,随着氯喹浓度的增加,ATP水平相应降低。氯喹在10~160 μmol/L浓度范围内,PI单染检测结果显示早 期凋亡率逐渐增加,转染miR-26b抑制剂可降低氯喹诱导的凋亡率。PCR检测结果表明,给予80 μmol/L氯喹作用后,miR-26b 的表达明显升高,Western blot检测Mcl-1蛋白的表达水平降低,转染miR-26b的抑制剂后表达升高。结论氯喹能诱导肝癌细 胞HepG2凋亡,且呈浓度依赖性,其机制可能是通过miR-26b靶向调控Mcl-1的表达实现的。
Abstract:
Objective To investigate the effect of chloroquine in inducing apoptosis of human hepatocellular carcinoma cells and explore the possible mechanism. Methods MTT assay and flow cytometry were used to evaluate chloroquine-induced growth inhibition and apoptosis in human hepatocellular carcinoma HepG2 cells, respectively. The ATP levels in chloroquinetreated cells were detected using an ATP assay kit. PCR and Western blotting were used to detect the expression levels of miR- 26b and Mcl-1 in the cells, respectively. Results Chloroquine inhibited the proliferation of HepG2 cells in a time- and concentration-dependent manner. Treatments with 80 μmol/L chloroquine for 24, 48, and 72 h induced survival rates of (71.59± 0.2)%, (45.40±0.5)%, and (26.34±1.4)% in the cells. Treatments with chloroquine at 40, 80, and 160 μmol/L for 5 h resulted in obviously lowered intracellular ATP levels in the cells to 87.80%, 71.29%, and 38.02% of the control level, respectively. At 80 μmol/L, chloroquine significantly increased the expression of miR-26b and down-regulated the expression of Mcl-1 in HepG2 cells, and the application of the miR-26b inhibitor increased the cellular expression of Mcl-1. Conclusions Chloroquine can inhibit the cell proliferation, reduce ATP level and induce apoptosis in HepG2 cells possibly through miR-26b-mediated regulation of Mcl-1.

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更新日期/Last Update: 1900-01-01