ADAM17基因siRNA诱导HepG2细胞凋亡,抑制增殖,增强染料木素对HepG2细胞的作用

Yongcun Liu , Zuoren Wang , Yuqiang Ji , Feng Li
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引用次数: 1

摘要

目的探讨ADAM17基因siRNA和染料木素对HepG2细胞凋亡和增殖抑制的影响,寻求治疗肝细胞癌的有效方法。方法将细胞分为对照组和实验组,分别用siRNA沉默ADAM17基因,单独沉默和与染料木素联合沉默。在几个时间段收集细胞并评估其增殖和凋亡情况。在治疗后24、48、72和96小时用MTT法检测细胞增殖,48小时用流式细胞术检测细胞凋亡。结果siRNA组在24h、48h和72h时细胞增殖明显受到抑制(P <0.05), 48 h细胞凋亡显著增加(P <0.01);染料木素组在24、48、72、96 h时细胞增殖均受到抑制,48 h时细胞凋亡率显著升高(P <0.01);而在siRNA转染和染料木素联合治疗组中,与单独治疗组相比,细胞增殖进一步显著减少,细胞凋亡增加。结论ADAM17基因可作为治疗肝癌的有效靶点,染料木素可作为治疗肝癌的有效药物。ADAM17基因siRNA和染料木素均能抑制HepG2细胞增殖,促进细胞凋亡,且两者联合处理的效果优于单独处理。
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siRNA of ADAM17 gene induces apoptosis, proliferation inhibition and enhances the effects of genistein on HepG2 cells

Objective

To investigate the effects of siRNA of ADAM17 gene and genistein on apoptosis and the inhibition of proliferation in HepG2 cells in an attempt to seek an effective therapy for hepatocellular carinoma.

Methods

Cells were divided into control groups and experimental groups and siRNA was used to silence the ADAM17 gene, alone and in combination with genistein. Cells were harvested at several time periods and assessed for proliferation and apoptosis. Proliferation was assayed by MTT at 24, 48, 72 and 96 hours following treatment and apoptosis was assessed by flow cytometric analysis at 48 hours.

Results

In siRNA groups, proliferation of cells was significantly inhibited compared to the control groups at 24, 48 and 72 hours(P < 0.05), and apoptosis was significantly increased at 48 hours(P < 0.01); In genistein groups, proliferation was inhibited at 24, 48, 72 and 96 hours, and the apoptosis ratio was significantly increased at 48 hours(P < 0.01); while in the groups that received the combination of siRNA transfection and genistein treatment, there was a further significant decrease of proliferation and increase in apoptosis compared with either treatment alone.

Conclusion

The ADAM17 gene could be an effective target, and genistein could be a useful agent, in the treatment of hepatocellular carcinoma. siRNA of ADAM17 gene and genistein both inhibited HepG2 cells proliferation and promoted apoptosis, and further, the combination of these treatments had a greater effect than either treatment alone.

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