摘要
目的探讨长链非编码RNA HOTAIR对人脑胶质瘤细胞侵袭的促进作用。方法采用HOTAIR-siRNA寡聚核苷酸转染胶质瘤U87和U251细胞系,通过实时荧光定量PCR技术检测HOTAIR在胶质瘤细胞中的表达水平。利用Western blot验证上皮间质化相关通路蛋白(Snail、Stat3和β-catenin)、标记蛋白(E-cadherin、CDH13和Vimentin)和侵袭迁移相关基质金属蛋白酶(MMP2、MMP9)的表达变化。采用Transwell实验,观察敲低HOTAIR后其对胶质瘤细胞侵袭的影响。结果下调HOTAIR表达后,U87和U251细胞的上皮间质化相关信号通路蛋白降低,E-cadherin和CDH13升高,Vimentin降低,MMP2和MMP9表达下降,细胞侵袭能力减弱(P<0.01)。结论 HOTAIR通过诱导上皮间质化促进了胶质细胞侵袭能力。
Objective To explore the promotive effect of long non-coding RNA（LncRNA）HOTAIR on the invasion of human glioma cells.Methods The HOTAIR-siRNA poligonucleotides were transfected into glioma cells U87 and U251.The expression of HOTAIR in human glioma cells was determined by qRT-PCR.The changes of epithelial-mesenchymal transition（EMT）-related signaling pathway proteins,marker proteins and matrix metalloproteinases in glioma cells were identified with Western blot.Matrigel invasion assay was applied to evaluate the invasive ability of U87 and U251cells.Results Downregulating the expression of HOTAIR could reduce EMT-related signaling pathway proteins of glioma cells,increase the epithelial cells marker proteins and decrease the mesenchymal cells marker protein,decrease MMP2 and MMP9 expressions,and reduce the invasive ability of glioma cells（P〈0.01）.Conclusion HOTAIR could promote the invasion of glioma cells by inducing EMT.
出处
《江苏医药》
CAS
2015年第4期373-376,共4页
Jiangsu Medical Journal
基金
国家自然科学基金(81272792
81372709)
江苏省"科教兴卫工程"医学重点学科(RC2011051)
