文章摘要
杨洪宝,张 海,冷 静.前列腺素E2对人肝细胞癌HepG2细胞E-cadherin表达的影响及其分子机制[J].南京医科大学学报,2009,29(3):281~285
前列腺素E2对人肝细胞癌HepG2细胞E-cadherin表达的影响及其分子机制
Studies on E-cadherin expression inducement of Prostaglandin E2 in HepG2 cells and its molecular mechanism
  
DOI:10.7655
中文关键词: 前列腺素E2  E-Cadherin  Akt
英文关键词: PGE2  E-cadherin  Akt
基金项目:国家自然科学基金资助(30470784,30871015)
作者单位
杨洪宝 南京医科大学肿瘤中心,病理学系,生殖医学重点实验室,江苏 南京 210029 
张 海  
冷 静  
摘要点击次数: 2366
全文下载次数: 1847
中文摘要:
      目的:研究前列腺素E2(PGE2)对人肝细胞癌HepG2细胞E-cadherin表达的调节作用及其分子机制,探讨其与肝癌侵袭转移的关系,为肝癌的治疗提供新的研究思路?方法:COX-2瞬时转染人肝细胞癌HepG2细胞,Western blot实验检测其E-cadherin表达的变化;PGE2及PI-3K抑制剂LY294002处理人肝细胞癌HepG2细胞,应用Western blot和RT-PCR分别测定肝癌细胞内E-cadherin蛋白水平和mRNA水平的变化,并观察60 min内Akt磷酸化水平的变化?结果:COX-2过表达转染HepG2细胞后,E-cadherin的表达明显降低;5?10?20 μmol/L PGE2处理HepG2细胞24 h后,E-cadherin表达水平与对照组比较分别下降了22.31%?36.3%?47.83%(P < 0.05);20 μmol/L PGE2处理HepG2细胞 24?48?72 h,E-cadherin蛋白和mRNA的表达与对照组比均明显降低(P < 0.01)?PI-3K抑制剂LY294002能部分阻断PGE2对E-cadherin表达的调节作用;经PGE2处理的HepG2细胞Akt磷酸化水平显著升高,并且在15 min时达到最高?结论:PGE2可以抑制人肝细胞癌HepG2细胞中E-cadherin的表达,并很可能通过激活Akt信号转导通路而发挥作用?
英文摘要:
      Objective:To investigate the effect of Prostaglandin E2 on expression of E-Cadherin in HepG2 cells and its molecular mechanism. Methods:HepG2 cells were transfected with PCDNA3-COX-2; HepG2 cells were treated with Prostaglandin E2 and PI-3K inhibitor LY294002. Western blotting was employed to detect E-cadherin expression and the expression of p-Akt. E-cadherin mRNA levels were examined by reverse transcription-PCR(RT-PCR). Results:COX-2 plasmid transfected HepG2 cells show greatly decreased level of E-cadherin expression. when HepG2 cells were treated with different concentration of PGE2 for 24 h, the expression level of E-cadherin was decreased in a dose-dependent manner. When treated with 20 μmol/L PGE2 for 24 h,48 h and 72h, the level of E-cadherin mRNA was decreased in a time-dependent manner. By using PI-3K inhibitor LY294002, we found LY294002 could partially block the effect of PGE2 on E-cadherin expression. Akt phosphorylation level was remarkably increased in HepG2 cells when treated with PGE2, and reached the highest level at 15 minutes. Conclusion:Prostaglandin E2 can repress E-cadherin expression in HepG2 cells, which is probably related to the Akt signal transduction pathway.
查看全文   查看/发表评论  下载PDF阅读器