上海交通大学学报（医学版）

上海交通大学学报（医学版） ›› 2018, Vol. 38 ›› Issue (10): 1145-.doi: 10.3969/j.issn.1674-8115.2018.10.002

• 论著·基础研究 • 上一篇    下一篇

三氧化二砷对肝细胞癌 HepG2细胞系作用效果的代谢组学研究

黄巾帼 1*，张海南 1*，陈子卿 1*，杨丽娜 2，郭书娟 1，陶生策 1   

  1. 1. 上海交通大学系统生物医学研究院，系统生物医学教育部重点实验室，上海 200240；2. 复旦大学附属肿瘤医院中西医结合科，上海 200032
  • 出版日期:2018-10-28 发布日期:2018-11-18
  • 通讯作者: 陶生策，电子信箱：taosc@sjtu.edu.cn。
  • 作者简介:黄巾帼（ 1993—），女，硕士生；电子信箱： huangjinguo@sjtu.edu.cn。张海南（ 1989—），女，博士生；电子信箱： zhanghainan.13@163.com。陈子卿（1990—），男，硕士生；电子信箱： chen.ziqing@ki.se。*为共同第一作者。
  • 基金资助:
    国家重点研发计划 (2016YFA0500600)；国家自然科学基金（ 31670831）

Metabolomics study of the effect of arsenic trioxide on hepatocellular carcinoma cell line HepG2

HUANG Jin-guo1*, ZHANG Hai-nan1*, CHEN Zi-qing1*, YANG Li-na2, GUO Shu-juan1, TAO Sheng-ce1   

  1. 1. Shanghai Center for Systems Biomedicine, Key Laboratory of Systems Biomedicine (Ministry of Education), Shanghai Jiao Tong University, Shanghai 200240, China; 2. Department of Integrative Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China
  • Online:2018-10-28 Published:2018-11-18
  • Supported by:
    National Key Research and Development Program of China, 2016YFA0500600; National Natural Science Foundation of China, 31670831

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摘要： 目的 ·从代谢组学的角度揭示三氧化二砷（ arsenic trioxide，ATO）对肝细胞癌（ hepatocellular carcinoma，HCC）的作用机制。方法 ·分别取 ATO处理 12、24和 36 h的肝细胞癌 HepG2细胞系，通过气相色谱 /质谱联用和液相色谱 /串联质谱联用对其代谢物谱进行全局性分析。结果 ·共检测到 307种代谢物。生物信息学分析表明，糖基化和单碳代谢是主要受影响的细胞功能。其他细胞功能或途径如线粒体脂肪酸 β-氧化、三羧酸循环、戊糖磷酸途径和谷胱甘肽代谢等也受到影响。结论 · ATO通过影响 HepG2细胞主要的代谢途径，抑制细胞生长和迁移，并加剧氧化应激来诱导癌细胞凋亡。

关键词: 砷剂, 三氧化二砷, 肝细胞癌, HepG2, 代谢组学

Abstract:

Objective · To reveal the mechanism of the effect of arsenic trioxide (ATO) on hepatocellular carcinoma (HCC) cells through metabolomics study. Methods · HCC cell line HepG2 was treated with ATO for 12 h, 24 h and 36 h respectively. The global metabolite profiles were monitoredmetabolomics analysis using GC/MS and LC/MS/MS. Results · A total of 307 certified metabolites were detected. Bioinformatics analysis showed that glycosylation and one-carbon metabolism were the main cellular functions that have been affected. Other affected cellular functions/pathways included mitochondrial function fatty acid β-oxidation, TCA cycle, pentose phosphate pathway (PPP) and glutathione metabolism. Conclusion · ATO treatment affects the main metabolomic pathway of HepG2, and inhibits cell growth and migration, then exacerbates oxidative stress to induce cancer cell apoptosis.

Key words: arsenic, arsenic trioxide, hepatocellular carcinoma, HepG2, metabolomics

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