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高尔基蛋白73参与炎症反应的分子机制研究

王翠 魏从文 邹德勇 刘丽萍 郝钦芳 丁琪 钟辉 杨晓莉

军事医学2016,Vol.40Issue(4):304-307,4.
军事医学2016,Vol.40Issue(4):304-307,4.DOI:10.7644/j.issn.1674-9960.2016.04.009

高尔基蛋白73参与炎症反应的分子机制研究

Molecular mechanism of Golgi protein 73 in inflammation

王翠 1魏从文 2邹德勇 3刘丽萍 4郝钦芳 4丁琪 4钟辉 4杨晓莉3

作者信息

  • 1. 安徽医科大学武警总医院临床学院,合肥 230032
  • 2. 武警总医院,北京 100039
  • 3. 军事医学科学院生物工程研究所,北京 100850
  • 4. 武警总医院,北京 100039
  • 折叠

摘要

Abstract

Objective To study the effect of Golgi protein 73(GP73) on inflammation, and to reveal the effect of GP73 on tumorigenesis and metastasis.Methods The transcriptional activity of NF-κB and the expression of IL-1β, IL-6 and TNF-αwith GP73 overexpression or knockdown were detected to illuminate the role of GP73 in inflammation.According to the TCGA database, the correlation between the transcriptional activity of GP73 and the expression of NF-κB, IL-1β, IL-6 and TNF-αwas analyzed to determine the role of GP73 in tumor inflammation.Results Correlative analysis showed that there was a positive correlation between the expression of GP73 with NF-κB, IL-1β, IL-6 and TNF-α.The transcriptional activity of NF-κB was upregulated by GP73 overexpression, but downregulated by GP73 knockdown.The expression of IL-1β, IL-6 and TNF-αwas upregulated by GP73 overexpression.Ammonium pyrrolidinedithiocarbamate ( PDTC ) was in-volved in inflammation reaction induced by GP73.Conclusion GP73 is possibly involved in inflammation and promotes tu-morigenesis and metastasis.

关键词

GP73/肿瘤/炎症/NF-κB/白细胞介素/肿瘤坏死因子α

Key words

GP73/neoplasm/inflammation/NF-κB/interleukin/tumor necrosis factorα

分类

医药卫生

引用本文复制引用

王翠,魏从文,邹德勇,刘丽萍,郝钦芳,丁琪,钟辉,杨晓莉..高尔基蛋白73参与炎症反应的分子机制研究[J].军事医学,2016,40(4):304-307,4.

基金项目

武警部队院级二类课题资助项目 ()

军事医学

OA北大核心CSCDCSTPCD

1674-9960

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