期刊文献+

环氧合酶2对肺癌细胞FOXC2的表达及侵袭能力的影响 被引量:2

Effect of cyclooxygenase-2 on FOXC2 expression and cell invasion of lung cancer cells
原文传递
导出
摘要 目的探讨环氧合酶2(COX-2)对肺癌细胞叉头框C2(FOXC2)的表达及侵袭能力的影响。方法采用COX-2过表达质粒、EP1受体过表达质粒及si-FOXC2转染人肺癌A549细胞,用前列腺素E2(PGE_2)及EP1受体激动剂17-PT-PGE_2处理细胞,检测FOXC2蛋白表达水平及细胞侵袭能力的变化。结果过表达COX-2后,FOXC2蛋白表达升高(P<0.05)。用不同浓度PGE_2处理细胞,FOXC2蛋白表达上调;其中,2.5μmol/L处理时上调最明显(P<0.01)。PGE_22.5μmol/L处理细胞后,细胞侵袭率升高(P<0.05),同时干扰FOXC2,细胞侵袭率下降(P<0.05)。用不同浓度17-PT-PGE_2处理细胞,FOXC2蛋白表达水平升高,其中5.0μmol/L处理时升高最明显(P<0.01)。过表达EP1受体后,FOXC2蛋白表达增加(P<0.05)。结论 COX-2能够通过激活EP1受体来促进FOXC2的表达,进而促进肺癌细胞的侵袭能力。 Objective To investigate the effect of cyclooxygenase-2(COX-2)on forkhead box C2(FOXC2)expression and cell invasion of lung cancer cells.Methods The human lung cancer A549 cells were transfected with COX-2 and EP1 receptor overexpression plasmid and si-FOXC2 and treated with PGE2 and EP1 receptor agonist 17-PT-PGE2.The protein expression of FOXC2 and cell invasion were detected.Results The protein expression of FOXC2 was increased after COX-2 overexpressed(P<0.05).The protein expression of FOXC2 was increased after treated with different concentrations of PGE2,which was obvious after treated with PGE2 2.5μmol/L(P<0.01).The cell invasion was higher after treated with PGE2 2.5μmol/L,which was lower after transfected with si-FOXC2 simultaneously(P<0.05).The protein expression of FOXC2 was increased after treated with different concentrations of 17-PT-PGE2,which was obvious after treated with 17-PT-PGE2 5.0μmol/L(P<0.01).The protein expression of FOXC2 was increased after overexpression of EP1 receptor(P<0.05).Conclusion COX-2 can promote the expression of FOXC2 by activating the EP1 receptor and the cell invasion of lung cancer cells.
作者 王中原 黄轶洲 黄可 陆晨妍 马倩雪 戴欣媛 白小明 WANG Zhongyuan;HUANG Yizhou;HUANG Ke(Basic Medical School,Nanjing Medical University, Nanjing 211166,CHINA)
出处 《江苏医药》 CAS 2018年第12期1373-1377,共5页 Jiangsu Medical Journal
基金 中国博士后科学基金(2016M600432)
关键词 环氧合酶2 叉头框C2 肺癌 细胞侵袭 Cyclooxygenase-2 Forkhead box C2 Lung cancer Cell invasion
  • 相关文献

同被引文献13

引证文献2

二级引证文献3

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部