期刊文献+

EGFR反义寡脱氧核苷酸硫代修饰片段调节人肝癌细胞中E-cadherin mRNA表达的研究 被引量:4

Modulation of Antisense Phosphorothioate Oligodeoxynucleotides of Epidermal Growth Factor Receptor on E-cadherin mRNA Expression in Human Hepatocellular Cell
暂未订购
导出
摘要 目的:研究表皮生长因子受体( epidermal growth factor receptor, EGFR)反义寡脱氧核苷酸硫代修饰片段对人肝癌细胞 E-cadherin基因表达调节。方法:应用逆转录聚合酶链反应( RT-PCR)方法。以 HPRT(hypoxanthine phosphoribosyltransferase)为内标,分析 3.2μ mol/L浓度的 EGFR反义寡脱氧核苷酸硫代修饰片段在作用 84 h时对人肝癌细胞基因 E-cadherin mRNA表达水平的影响。结果: EGFR反义寡脱氧核苷酸硫代修饰片段有明显的刺激人肝癌细胞表达 E-cadherin的作用,与正常对照组相比,其 E-cadherin mRNA表达水平增高约 66.36%( P< 0.05)。结论: EGFR反义寡脱氧核苷酸硫代修饰片段是人肝癌细胞表达 E-cadherin基因的调节剂,能刺激人肝癌细胞 E-cadherin基因的表达 ;本研究为预防和治疗肝癌的侵袭转移提供了新的途径和方法。 Objectives: This study was designed to investigate modulation of phosphorothioate oligodeoxynucleotides(S-ODNs) of EGFR on E-cadherin mRNA expression in human hepatocellular carcinoma cells. Methods: Treated with concentration of 3.2μ mol/L S-ODNs in culture medium, the relative E-cadherin mRNA level at 84 hour in human hepatocellular carcinoma cells was evaluated by reverse-transcriptase polymerase chain reaction with using HPRT (hypoxanthine phosphoribosyltransferase) as an internal control standard. Result: The expression of E-cadherin gene mRNA was enhanced obviously by S-ODNs. Compared with control group, the relative expression level of E-cadherin gene mRNA was increased at about 66.36% (P< 0.05). Conclusion: S-ODNs is the regulator of E-cadherin gene expression, it can enhanced E-cadherin gene expression in human hepatoma cells. Understanding the regulation of E-cadherin gene expression in human hepatocellular carcinoma cells might contribute to development of a new preventive and therapeutic strategy for tumor invasiveness.
出处 《癌症》 SCIE CAS CSCD 北大核心 2001年第3期255-257,共3页 Chinese Journal of Cancer
关键词 表皮生长因子受体 硫代磷酸酯寡脱氧核苷酸 钙粘蛋白 肝癌细胞 逆转录聚合酶链反应 MRNA E-CADHERIN : Epidermal growth factor receptor Phosphorothioate oligodeoxynucleotides Hepatocellular carcinoma cells Reverse-transcriptase polymerase chain reaction E-cadherin.
  • 相关文献

参考文献1

共引文献14

同被引文献74

引证文献4

二级引证文献29

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