期刊文献+

人白细胞介素-33在肾细胞癌中高表达并通过EMT促进肾癌细胞的侵袭能力 被引量:3

High expression of interleukin-33 in renal cell carcinoma which promoting cell invasion by EMT
下载PDF
导出
摘要 目的:研究人白细胞介素(interleukin,IL)-33在肾细胞癌中的表达情况及在肾癌细胞786-0侵袭中的作用。方法:应用免疫组化法检测34例不同级别肾脏细胞癌患者肾脏肿瘤组织及癌旁组织中IL-33表达水平;应用细胞侵袭实验检测IL-33对肾癌细胞786-0侵袭的影响;应用Western blot检测IL-33对肾癌细胞786-0上皮细胞间质转化(epithelial-mesenchymal transition,EMT)相关蛋白表达的影响。结果:免疫组化结果显示,与癌旁组织相比,肾细胞癌患者肿瘤组织中IL-33水平明显升高,半定量统计分析结果表明两者间存在统计学差异(P<0.001)。体外实验表明,IL-33可促进786-0细胞侵袭;Western blot结果显示,用IL-33刺激786-0细胞后细胞内E-cadherin蛋白表达量明显降低,而vimentin蛋白表达量明显升高。结论:IL-33在肾细胞癌组织中表达明显升高,并可能通过诱导肾癌细胞发生EMT进而提高肾癌细胞的侵袭能力。 Objective:To detect the expression of interleukin(IL)-33 in renal cell carcinoma(RCC) and its effect on invasion of human 786-0 cells.Methods:IL-33 protein in 34 patients with different grades of RCC tissues and para-adjacent tissues was detected with immunohistochemistry assay.Transwell invasion assay was used to investigate the effect of IL-33 on invasion of 786-0 cells.Western blot assay was conducted to detect the markers of epithelial-mesenchymal transition(EMT) in 786-0 cells after IL-33 treatment.Results:IL-33 protein expression was significantly higher in RCC tissues compared to para-adjacent renal tissues(P〈0.001).IL-33 enhanced 786-0 cells invasion in vitro.Moreover,the expression of E-cadherin was significantly decreased while the expression of vimentin was significantly increased after IL-33 treatment.Conclusion:IL-33 is overexpressed in RCC tissues and may contribute to renal cancer cells invasion by inducing EMT.
出处 《南京医科大学学报(自然科学版)》 CSCD 北大核心 2017年第4期409-412,共4页 Journal of Nanjing Medical University(Natural Sciences)
基金 国家自然科学基金(81372397) 临床医学研究中心2013(ZX13)
关键词 人白细胞介素-33 肾细胞癌 侵袭 上皮细胞间质转化 interleukin-33 renal cell carcinoma invasion epithelial-mesenchymal transition
  • 相关文献

参考文献3

二级参考文献57

  • 1Li C, Yang CW. The pathogenesis and treatment of chronicallograft nephropathy [J]. Nat Rev Nephrol,2009,5 (9):513-519.
  • 2Mas VK, Archer KJ , Scian M,el al. Molecular pathwaysinvolved in loss of graft function in kidney transplant re-cipients [J]. Expert Kev Mol Diagn,2010,10 (3):269-284.
  • 3Strutz F. Pathogenesis of tuhulointei'stitial fibrosis inchronic allograft dysfunction [J]. Clin Transplant,2009,23(Suppl 21):26-32.
  • 4Comaire E,Duhois-Xu YC,Rondeau E,et al. Interstitialfibrosis in renal grafts : On the way to a better detection[J]. Nephrol Ther,2010,6(6) :494-498.
  • 5Zeisherg EM,Tamavski O’Zeisherg M,et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis[J]. Nat Med,2007,13(8) :952-961.
  • 6Zeisberg EM,Potenta S,Xie L,et al. Discovery of en-dothelial to mesenchymal transition as a source for carci-noma-associated fibroblasts [J]. Cancer Res,2007,67(21):10123-10128.
  • 7Hashimoto N, Phan SH,Imaizumi K,et al. En dothelia]-mesenchymal transition in bleomycin-induced pulmonaryfibrosis [ J]. Am J Hespir Cell Mo] Biol,2010,43 (2):161-172.
  • 8Sumioka T,Ikeda K,Okada Y,et al. Inhibitory effect ofblocking TGF-beta/Smad signal on injury-induced fibro-sis of corneal endothelium [J]. Mol Vi,2008,14 (3):2272-2281.
  • 9Kitao A,Sato Y,Sawada-Kitamura S,et al. Endothelial tomesenchymal transition via transforming growth factor-betal/Smad activation is associated with portal venousstenosis in idiopathic portal hypertension [J]. Ame JPathol,2009,175(2) :616-626.
  • 10Potenta S,Zeisberg E, Kalluri R. The role of endothelial-to-mesenchymal transition in cancer progression [J], Br JCancer,2008,99(9) : 1375-1379.

共引文献4

同被引文献11

引证文献3

二级引证文献13

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