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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 investigate the role of long chain non-coding RNA HOTAIR in the invasion of human glioma cells. Methods HOTAIR-siRNA oligonucleotides were transfected into glioma U87 and U251 cell lines. The expression of HOTAIR in glioma cells was detected by real-time fluorescence quantitative PCR. The expressions of Snail, Stat3 and β-catenin, E-cadherin, CDH13 and Vimentin and the expressions of matrix metalloproteinase (MMP2, MMP9) in invasion and migration were detected by Western blot. Transwell experiments were performed to observe the impact of HOTAIR knockdown on glioma cell invasion. Results After down-regulation of HOTAIR expression, the protein expression of epithelial-mesenchyme-related signal pathway in U87 and U251 cells was decreased, while E-cadherin and CDH13 were increased, Vimentin was decreased, MMP2 and MMP9 expressions were decreased, and cell invasive ability was weakened (P <0.01). Conclusion HOTAIR promotes glial cell invasion by inducing epithelial-mesenchymal transition.