Galangin inhibits proliferation of hepatocellular carcinoma cells by inducing endoplasmic reticulum stress.

Lijuan Su, Xiaoyi Chen, Jun Wu, Biyun Lin, Haitao Zhang, Liubo Lan, Hui Luo
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引用次数: 60

Abstract

Prolonged endoplasmic reticulum (ER) stress may activate apoptotic pathways in cancer cells. It is suggested that ER stress has the potential of enhancing tumor death in cancer therapy. Galangin, a flavonol derived from Alpinia officinarum Hance, has been shown to suppress the proliferation of hepatocellular carcinoma cells (HCC). The aim of this study was to determine whether galangin was able to induce ER stress in HepG2, Hep3B and PLC/PRF/5 cells. The proliferation of HCC was tested by MTT method. Intracellular Ca(2+) levels were measured with Fluo3-AM.The proteins levels of GRP94, GRP78 and CHOP were detected by Western blot. To further understand the anti-HCC mechanism of galangin, mitogen-activated protein kinases (MAPKs) were detected. The results showed that galangin treatment induced ER stress was evidenced by increased protein levels of GRP94, GRP78 and CHOP, as well as increased free cytosolic Ca(2+) concentration. ER stress inhibitor 4-PBA and CHOP siRNA blocked significantly galangin-induced ER in all three cell lines. Further experiments showed that MAPKs involved in ER stress induced by galangin. In summary, galangin is identified as a stimulator of ER stress to suppress the proliferation of HCC, and may be used as a potential anti-cancer agent.

高良姜通过诱导内质网应激抑制肝癌细胞增殖。
延长内质网应激可激活癌细胞凋亡通路。提示内质网应激在肿瘤治疗中具有提高肿瘤死亡的潜力。高良姜是一种从高良姜中提取的黄酮醇,已被证明可以抑制肝细胞癌细胞(HCC)的增殖。本研究的目的是确定高良姜是否能够诱导HepG2、Hep3B和PLC/PRF/5细胞的内质网应激。MTT法检测肝细胞癌的增殖情况。用Fluo3-AM测定细胞内Ca(2+)水平。Western blot检测GRP94、GRP78、CHOP蛋白表达水平。为了进一步了解高良姜的抗hcc机制,我们检测了丝裂原活化蛋白激酶(MAPKs)。结果表明,高蒋素处理诱导内质网应激表现为GRP94、GRP78和CHOP蛋白水平升高,胞浆游离Ca(2+)浓度升高。内质网应激抑制剂4-PBA和CHOP siRNA在所有三种细胞系中均显著阻断高良姜诱导的内质网。进一步的实验表明,MAPKs参与高良姜诱导的内质网应激。综上所述,高良姜可以刺激内质网应激,抑制HCC的增殖,可能是一种潜在的抗癌药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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