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索拉非尼对肝癌细胞中PD-L1表达的影响及机制

刘林森 龙文汀 张悦 刘树旺 刘利平

山东医药2017,Vol.57Issue(29):5-7,3.
山东医药2017,Vol.57Issue(29):5-7,3.DOI:10.3969/j.issn.1002-266X.2017.29.002

索拉非尼对肝癌细胞中PD-L1表达的影响及机制

Effect of sorafenib on expression of PD-L1 in hepatocellular carcinoma cells

刘林森 1龙文汀 2张悦 1刘树旺 1刘利平1

作者信息

  • 1. 深圳市人民医院·暨南大学第二临床医学院,广东深圳 518020
  • 2. 北京大学深圳医院
  • 折叠

摘要

Abstract

Objective To investigate the effect of sorafenib on the expression of programmed cell death ligand 1(PD-L1) in the hepatocellular carcinoma cells and the underlying mechanism.Methods Real-time PCR and Western blotting was applied to detect the mRNA and protein expression levels of PD-L1 and hypoxia-inducible factor-1α (HIF-1α) in HepG2 cells treated with 0, 2.5, 5, 10 μmol/L sorafenib, respectively.HepG2 cells were transfected with pEGFP-N1-HIF-1α (pEGFP-N1-HIF-1α group), shRNA-HIF-1α (shRNA-HIF-1α group) and the control plasmids including pEGFP-N1 and shRNA-control (pEGFP-N1 group, shRNA-control group), and then the mRNA and protein expression levels of HIF-1α and PD-L1 were detected.Results The mRNA and protein expression levels of PD-L1 and HIF-1α in HepG2 cells were down-regulated after sorafenib intervention in a dose-dependent manner (both P<0.05).Compared with the pEGFP-N1 group, the mRNA and protein expression levels of PD-L1 and HIF-1α increased in the pEGFP-N1-HIF-1α group (both P<0.01).Meanwhile, compared with the shRNA-control group, the mRNA and protein expression levels of PD-L1 and HIF-1α significantly decreased in the shRNA-HIF-1α group (both P<0.01).Conclusions Sorafenib can inhibit the expression of PD-L1 in liver cancer cells through inhibiting HIF-1α signaling pathway.

关键词

肝肿瘤/索拉非尼/程序性死亡分子配体1/缺氧诱导因子1α

Key words

liver neoplasms/sorafenib/programmed cell death ligand 1/hypoxia-inducible factor-1α

分类

医药卫生

引用本文复制引用

刘林森,龙文汀,张悦,刘树旺,刘利平..索拉非尼对肝癌细胞中PD-L1表达的影响及机制[J].山东医药,2017,57(29):5-7,3.

基金项目

国家自然科学基金青年基金项目(81402041) (81402041)

深圳市科技创新项目(JCYJ20160422170206664,JCYJ20150403101028198). (JCYJ20160422170206664,JCYJ20150403101028198)

山东医药

OACSTPCD

1002-266X

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