首页|紫草素抑制肝癌细胞增殖的机制研究

紫草素抑制肝癌细胞增殖的机制研究

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目的 探讨紫草素抑制肝细胞肝癌(HCC)细胞增殖的分子机制.方法 将人HCC细胞株HepG2分为对照组、紫草素低剂量组、紫草素高剂量组和miR-181c空白组、miR-181c抑制组和miR-181c转染组,培养基中分别加入工作浓度为2.5和5.0 μmol/L紫草素溶液以及miR-181c抑制物和miR-181c模拟物转染处理.采用细胞计数(CCK-8)法检测细胞增殖率,流式细胞术检测细胞凋亡率;qRT-PCR法检测细胞中miR-181c和非染色体结构维护凝缩蛋白I复合体G亚基(NCAPG)mRNA相对表达量,Western blot法检测细胞NCAPG和B淋巴细胞瘤-2(Bcl-2)蛋白相对表达量.结果 与对照组相比,高剂量组、低剂量组细胞增殖率显著降低(均P<0.05);与低剂量组相比,高剂量组显著降低(P<0.05).与miR-181c空白组相比,miR-181c抑制组细胞增殖率显著升高,miR-181c转染组显著降低(均P<0.05).高剂量组细胞凋亡率明显高于低剂量组和对照组(均P<0.05);与miR-181c空白组相比,miR-181c抑制组细胞凋亡率显著降低(P<0.05),miR-181c转染组显著升高(P<0.05).高剂量组miR-181c mRNA相对表达量明显高于低剂量组和对照组(均P<0.05);与miR-181c空白组相比,miR-181c抑制组miR-181c mRNA相对表达量显著降低(P<0.05),miR-181c转染组显著升高(P<0.05).高剂量组NCAPG mRNA相对表达量、NCAPG和Bcl-2蛋白相对表达量均明显低于低剂量组和对照组(均P<0.05);与miR-181c空白组相比,miR-181c抑制组NCAPG mRNA相对表达量、NCAPG和Bcl-2蛋白相对表达量均显著升高(P<0.05),miR-181c转染组均显著降低(均P<0.05).结论 紫草素可上调HCC细胞中miR-181c表达从而抑制其增殖.
Mechanism of shikonin inhibiting the proliferation of hepatocellular carcinoma cell
Objective To investigate the molecular mechanism of shikonin in inhibiting the proliferation of hepatocellular carcinoma(HCC)cells.Methods HepG2 human HCC cells were divided into six groups:control,low-dose shikonin,high-dose shikonin,miR-181c negative control(NC),miR-181c-inhibitor,and miR-181c-mimic groups.Cells were treated respectively with 2.5 or 5.0 μmol/L concentrations of shikonin,and transfected with miR-181c inhibitor or miR-181c mimics,respectively.Cell proliferation was detected using the cell counting kit-8(CCK-8)assay,while apoptosis was assessed by flow cytometry.The relative mRNA expression levels of miR-181c and non-SMC condensin I complex subunit G(NCAPG)were measured by qRT-PCR,and the relative protein expression levels of NCAPG and B-cell lymphoma 2(Bcl-2)were determined by Western blot.Results Compared with the control group,the cell proliferation rate was significantly reduced in both the high-dose and low-dose shikonin groups(both P<0.05),and that of the high-dose group reduced more remarkably than the low-dose group(P<0.05).In comparison to the miR-181c NC group,the cell proliferation rate significantly increased in the miR-181c inhibitor group,while significantly decreased in the miR-181c mimic group(both P<0.05).The high-dose group exhibited a significantly higher apoptosis rate than both the low-dose group and control group(both P<0.05).Compared with the miR-181c NC group,the apoptosis rate significantly decreased in the miR-181c inhibitor group,while significantly increased in the miR-181c mimic group(both P<0.05).The relative expression level of miR-181c mRNA in the high-dose group was significantly higher than that of the low-dose and control groups(both P<0.05).Compared to the miR-181c NC group,the miR-181c mRNA relative expression level significantly decreased in the miR-181c inhibitor group,while significantly increased in the miR-181c mimic group(both P<0.05).The relative expression levels of NCAPG mRNA,NCAPG and Bcl-2 proteins in the high-dose group were significantly lower than those of the low-dose group and control group(all P<0.05).Compared to the miR-181c NC group,the relative expression levels of NCAPG mRNA,NCAPG and Bcl-2 proteins significantly increased in the miR-181c inhibitor group,while significantly decreased in the miR-181c mimic group(all P<0.05).Conclusion Shikonin can upregulate miR-181c expression in HCC cells,thereby inhibiting the proliferation of HCC cells.

ShikoninmiR-181cHepatocellular carcinomaCell proliferation

叶亚丽、陈美云、朱立飞、陈景丹

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317100 台州,三门县人民医院检验科

317100 台州,三门县人民医院感染科

紫草素 miR-181c 肝细胞肝癌 细胞增殖

台州市科技计划项目台州市科技计划项目

21ywb15720ywb188

2024

浙江医学
浙江省医学会

浙江医学

CSTPCD
影响因子:0.428
ISSN:1006-2785
年,卷(期):2024.46(14)
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