| 杨 澜,邓兴明,李 贝,邓雪松,陆菁潇,吕国庆.多组学分析揭示Grb2介导α-硫辛酸抑制肝癌细胞增殖研究[J].现代生物医学进展英文版,2018,(20):3817-3823. |
| 多组学分析揭示Grb2介导α-硫辛酸抑制肝癌细胞增殖研究 |
| Multi-omics Analyses Reveal α-lipoic acid-regulated Cell Proliferation via Grb2-mediated Signaling Downregulation |
| Received:May 30, 2018 Revised:June 23, 2018 |
| DOI：10.13241/j.cnki.pmb.2018.20.004 |
| 中文关键词: α-硫辛酸 肝细胞癌 细胞增殖 Grb2 |
| 英文关键词: Alpha lipoic acid, Hepatocellular carcinoma, Cell proliferation, Growth factor receptor-bound protein 2 |
| 基金项目:国家自然科学基金面上项目（81672813）；人事部中国博士后科学基金项目（2016M602594）；深圳市科技计划2016年基础研究项目（JCYJ20160425105945739）；深圳市"三名工程"（SZSM201612051） |
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| 中文摘要: |
| 摘要 目的：为更深入了解α-硫辛酸如何影响复杂信号通路间的相互作用抑制细胞增殖。方法：我们凭借RNA-Seq与同位素相对标记与绝对定量技术，对α-LA处理24 h HepG2细胞在转录和蛋白表达水平的变化差异进行分析，并借助实时定量PCR免疫印迹技术对组学数据进行了鉴定。结果：转录组学提示共有4,446个基因（2,097个基因表达下调，2,349个基因表达上调）的表达在α-LA处理24 h后呈现显著性改变。GO分析提示，编码肿瘤相关细胞膜蛋白的基因是受α-LA影响最为显著的一类mRNA；蛋白质组学进一步提示Grb2可能是受α-LA调控的膜受体信号通路中关键的靶分子。结论：α-LA抑制HCC细胞增殖是通过下调Grb2介导的相关通路而实现。 |
| 英文摘要: |
| ABSTRACT Objective: To more comprehensively understand how a-LA mediates the components of the complex web of interactions among the signalling pathways to repression the cell proliferation. Methods: In this study, we combined the use of an RNA sequencing (RNA-Seq) database and isobaric tag for relative and absolute quantitation (iTRAQ)-based quantitative proteomics data to investigate the dynamic genomic/proteomic response of HepG2 cells to α-LA stress. Real-time PCR and western blotting were used to identified the expression changes of key genes which from the omics. Results: A total of 4,446 differentially expressed genes (2,097 downregulated and 2,349 upregulated) were identified via RNA-Seq in HepG2 cells after exposure to α-LA for 24 h. Moreover, GO analyses showed mRNA that encode cancer-relevant cell membrane proteins were significantly affected. A further proteomic analysis predicted that Grb2 may mediate the key target pathways activated by exposure to α-LA. Conclusion: These findings provide a novel mechanism by which α-LA regulates cell proliferation via the downregulation of growth factor-stimulated Grb2 signaling. |
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