期刊文献+

Kruppel样因子在人食管癌细胞中的作用研究

Effects of Kruppel like factor on human esophageal cancer cells
下载PDF
导出
摘要 目的探讨Kruppel样因子(KLF4)对食管癌细胞生长、侵袭及迁移等生物学行为的影响,揭示其与食管癌发生发展的关系。方法检测人食管癌细胞株KYSE140、KYSE150、EC109及EC9706及食管永生化细胞NE3中KLF4的表达,通过siRNA的方法将KLF4高表达的KYSE140细胞敲降KLF4基因,通过MTT试验、软琼脂集落形成实验、Transwell小室侵袭实验检测该细胞生物学行为的变化。结果与转染control siRNA的细胞相比,转染KLF4-siRNA1、KLF4-siRNA2的KYSE140细胞生长速度上升,细胞穿过Transwell微孔膜的细胞数量增加,并且形成的集落明显增加,差异均有统计学意义(P<0.05)。结论 KLF4在人食管癌细胞的增殖、侵袭和迁移过程中起着负性调节的作用,可能成为早期诊断和判断食管癌预后的分子标志物以及临床治疗的分子靶点。 Aim To investigate the effect of Kruppel like factor 4 ( KLF4 ) on esophageal cancer cell growth, invasion and migration, and reveal its relationship with the occurrence and development of human esophageal cancer. Methods Expression of KLF4 was detected in the esophageal cancer cell lines, including KYSE140, KYSE150, EC109 and EC9706, and immortalized esophageal cell NE3. KLF4 highly expressed KYSE140 cell was chosen to demonstrate the biological behavior changes after silencing the KLF4 with siRNA transfection by MTT test, colony formation test, and Transwell cell invasion assay. Results KLF4-siRNA1 and KLF4-siRNA2 transfected KYSE140 cells accelerated the proliferation and amount of Ttranswell invasion ceils and the colony formation increased. There was statistically significant difference between the siRNA transfected and control cells ( P 〈 0.05 ). Conclusion KLF4 negatively regulated the proliferation, invasion and migration of esophageal cancer cells, and it may be served as an emerging molecular biomarker for early diagnosis and therapeutic target for esophageal cancer.
出处 《中国药理学通报》 CAS CSCD 北大核心 2013年第5期729-733,共5页 Chinese Pharmacological Bulletin
基金 广东省自然科学基金项目(No 10451008901005515)
关键词 Kruppel样因子 食管癌 侵袭 迁移 增殖 细胞株 Kruppel like factor esophageal cancer invasion migration proliferation cell lines
  • 相关文献

参考文献3

二级参考文献174

  • 1张玉军,刘淑霞,齐凤英,左连富,郭建文.戊地昔布诱导人食管癌Eca109细胞凋亡的机制研究[J].中国药理学通报,2006,22(5):629-633. 被引量:9
  • 2李军霞,杲海霞,陈雪彦,王永利.戊地昔布抑制Lewis肿瘤生长的作用[J].中国药理学通报,2006,22(8):998-1001. 被引量:7
  • 3Spugnini E P, Porrello A, Citro G, et al. COX-2 overexpression in canine tumors : potential therapeutic targets in oncology [ J ]. Histol Histopathol, 2005,20:1309 - 12.
  • 4Konturek P C, Rembiasz K, Bumat G, et al. Effects of cyclooxygenase-2 inhibition on serum and tumor gastrins and expression of apoptosis-related proteins in coloreetal eancer[J]. Dig Dis Sci,2006, 51:779 - 87.
  • 5Shimizu D, Vallbohmer D, Kuramochi H, et al. Increasing eyelooxygenase-2 (cox-2) gene expression in the progression of Barrett's esophagus to adenocarcinoma correlates with that of Bcl-2 [ J]. lnt J Cancer,2006,17 ( 2 ) : 189 - 92.
  • 6Shamma A, Yamamoto H, Doki Y, et al. Up-regulation of cyclooxygenase-2 in squamous carcinogenesis of the esophagus [ J ]. Clin Cancer Res ,2000,6(4) : 1229 - 38.
  • 7Nishioka K, Doki Y, Miyata H, et al. Bile Acid promotes the proliferation of squamous cell carcinoma of the esophagus, independent of its inducing COX-2 expression [ J ]. J Surg Res, 2006,132 : 130 -5.
  • 8Du A ,Zhao B, Miao J, et al. Safrole oxide induces apoptosis by upregulating Fas and FasL instead of integrin beta4 in A549 human lung cancer ceils [ J ]. Bioorg Med Chem,2006,14:2438 - 45.
  • 9Cho S D,Ahn N S,Jung J W,et al. Critical role of the c-JunNH2- terminal kinase and p38 mitogen-activated protein kinase pathways on sodium butyrate-induccd apoptosis in DU145 human prostate cancer cells[ J]. Eur J Cancer Prev ,2006 ,15 : 57 -63.
  • 10Takahashi K, Yamanaka S. Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors. Cell 2006; 126:663-676.

共引文献68

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