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表皮生长因子对Hela细胞紧密连接蛋白3表达的影响及其可能机制

刘芳 桂定清 张力忆

中国现代医学杂志2018,Vol.28Issue(15):16-20,5.
中国现代医学杂志2018,Vol.28Issue(15):16-20,5.DOI:10.3969/j.issn.1005-8982.2018.15.004

表皮生长因子对Hela细胞紧密连接蛋白3表达的影响及其可能机制

Effect of epidermal growth factor on expression of Claudin-3 in Hela cells

刘芳 1桂定清 1张力忆1

作者信息

  • 1. 四川省达州市中心医院 妇产科,四川 达州 635000
  • 折叠

摘要

Abstract

Objective To investigate the effect of epidermal growth factor (EGF) on expression of Claudin-3 in Hela cells. Methods Hela cells were cultured to adherent growth. In the first group, cells were treated with different concentration of EGF for 8 hours (0, 0.5, 5.0, 10.0, 100.0 ng/ml). In the second group, cells were treated with 10 ng/ml EGF for different time of duration (0 min, 10 min, 30 min, 1 h, 2 h, 4 h, 8 h and 24 h). In the third group, cells were treated with antagonist of EGFR, phosphatidylinositol-3-kinase (PI3-K), mitogen-activated protein kinase (MAK), p38, or c-Jun N-terminal kinase (JNK) followed by treatment of 10 ng/ml EGF for 24 h. Expression of Claudin-3 was identified on protein and mRNA level. Phosphorylation of EGF signal pathway related proteins were tested. Results EGF promoted expression of Claudin-3 in time-dependent manner, and optimistic dose was 10 ng/ml. Phosphorylation of EGFR, protein kinase B (AKT), extracellular regulated protein kinase 1/2 (ERK1/2), p38 and JNK were significantly upregulated after EGF stimulation, which was reversed by all molecular inhibitors. Blockage of EGFR, PI3-K, MAPK, p38 and JNK effectively ameliorated EGF induced increase of Claudin-3 protein. Conclusion EGF increases expression of Claudin-3 in Hela cells through EGFR, PI3-K, MAPK, p38 and JNK signaling pathways.

关键词

表皮生长因子/紧密连接蛋白3/宫颈癌/促分裂素原活化蛋白激酶/细胞外调节蛋白激酶/磷脂酰肌醇3-激酶/蛋白激酶B/p38/c-Jun氨基末端激酶

Key words

epidermal growth factor/claudin-3/cervical cancer/MAPK/ERK/PI3-k/AKT/p38/JNK

分类

医药卫生

引用本文复制引用

刘芳,桂定清,张力忆..表皮生长因子对Hela细胞紧密连接蛋白3表达的影响及其可能机制[J].中国现代医学杂志,2018,28(15):16-20,5.

基金项目

四川省卫生和计划生育委员会科研课题(No:150055) (No:150055)

中国现代医学杂志

OACSTPCD

1005-8982

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