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竹荪多糖对人肝癌细胞系HCC-LM3的抑制作用

Inhibition Effect of Dictyophora Polysaccharides on Human Hepatocellular Carcinoma Cell Line HCC-LM3.

作者信息

Hu Ting, Zhang Kaiju, Pan Di, Pan Xueli, Yang Hongyan, Xiao Jiayan, Shen Xiangchun, Luo Peng

机构信息

School of Public Health, Guizhou Medical University, Guiyang, Guizhou, China (mainland).

The Key Laboratory Environmental Pollution and Disease Monitoring, Ministry of Education, Guizhou Medical University, Guiyang, Guizhou, China (mainland).

出版信息

Med Sci Monit. 2020 May 6;26:e918870. doi: 10.12659/MSM.918870.

DOI:10.12659/MSM.918870
PMID:32374722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7222657/
Abstract

BACKGROUND It has been reported that polysaccharides have potential novel anti-cancer properties. Previously, we confirmed that Dictyophora polysaccharides could significantly inhibit liver transplantation tumors in mice. However, the mechanism of Dictyophora polysaccharide action on human liver cancer is unclear. Here, we aimed to clarify the mechanism of Dictyophora polysaccharide action on human hepatocellular carcinoma cells, namely the effect on cell proliferation, the cell cycle, and apoptosis, and on the apoptosis-related genes and proteins in vitro. MATERIAL AND METHODS The HCC-LM3 cell line was incubated with 2.5 mg/mL Dictyophora polysaccharides for 24, 48, and 72 h. The cell growth inhibition rate was evaluated using Cell Counting Kit-8. Cell cycle and apoptosis were measured with flow cytometry. The expression of apoptosis-related genes and proteins was measured using real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. RESULTS The Dictyophora polysaccharides inhibited HCC-LM3 cell proliferation in a time- and dose-dependent manner and blocked the cell cycle in the G₂/M phase. In addition, Bax and caspase-3 expression were significantly increased after Dictyophora polysaccharides treatment. CONCLUSIONS To the best of our knowledge, this is the first published study on the mechanism of Dictyophora polysaccharide inhibition of HCC-LM3 cell proliferation.

摘要

背景 据报道,多糖具有潜在的新型抗癌特性。此前,我们证实竹荪多糖可显著抑制小鼠肝移植瘤。然而,竹荪多糖对人肝癌作用的机制尚不清楚。在此,我们旨在阐明竹荪多糖对人肝癌细胞作用的机制,即其对细胞增殖、细胞周期、凋亡以及体外凋亡相关基因和蛋白的影响。

材料与方法 将HCC-LM3细胞系与2.5 mg/mL竹荪多糖孵育24、48和72小时。使用细胞计数试剂盒-8评估细胞生长抑制率。通过流式细胞术检测细胞周期和凋亡情况。分别使用实时荧光定量聚合酶链反应(RT-qPCR)和蛋白质印迹法检测凋亡相关基因和蛋白的表达。

结果 竹荪多糖以时间和剂量依赖性方式抑制HCC-LM3细胞增殖,并将细胞周期阻滞在G₂/M期。此外,竹荪多糖处理后,Bax和caspase-3的表达显著增加。

结论 据我们所知,这是关于竹荪多糖抑制HCC-LM3细胞增殖机制的首次发表研究。

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