中文摘要：

目的采用shRNA ATB敲减胶质瘤U87细胞中ATB后,研究其对人胶质瘤细胞增殖、迁移和侵袭的影响。方法本研究采用实时定量PCR（qRT-PCR）方法检测ATB在人胶质瘤细胞系U87与正常人脑胶质细胞HEB中的表达情况。并在此基础上构建了ATB表达载体shRNA ATB质粒,利用其转染人胶质瘤U87细胞株,获取低表达ATB的U87细胞。应用MTT法检测敲减ATB后对U87细胞增殖的影响;应用细胞克隆实验检测敲减ATB后对U87细胞克隆增殖能力的影响;应用Transwell实验检测敲减ATB后对U87细胞迁移和侵袭能力的影响。结果 qRT-PCR结果显示,与正常人脑胶质细胞HEB相比,人脑胶质瘤细胞系U87中ATB表达明显上调（P〈0.01）;与shRNA对照组相比,转染了shRNA-ATB实验组能显著减少ATB水平（P〈0.01）;细胞克隆实验显示shRNA-ATB实验组细胞克隆形成能力较shRNA对照组明显降低（P〈0.01）;MTT结果表明敲减细胞内ATB后细胞增殖的速率明显低于shRNA对照组（P〈0.01）。此外,Transwell实验进一步验证了敲减胶质瘤U87细胞中的ATB后,细胞迁移和侵袭能力明显受到抑制（P〈0.01）。结论靶向敲减U87细胞中的ATB后能够抑制其增殖、迁移和侵袭,表明ATB基因可能是胶质瘤患者的潜在治疗靶点。

英文摘要：

Objective To investigate the effects of long non-coding RNA activated by TGF-p（ATB） on the prolif-eration, migration and invasion of human U87glioma cell line. Methods The expression of ATB inhuman U87 gli-oma cell line and human normal astrocyte （ HEB ） were detected by real-time quantitative PCR（ qRT-PCR） . And based on this, shRNA ATB plasmid were constructed ,which could knockdown ATB expression after transfected in-to U87 cells. The proliferation ability of cell was investigated through MTT assay and the colony-formation ability was tested by the cell cloning assay. Cell migration and invasion were measured by non-Matrigel transwell assay and Matrigel transwell assay in v i tro . Results Using q R T - P C R analysis, w e found ATB expression levels in U 8 7 cell line was significantly increased compared with HEB（P 〈0. 01 ）. The expression of ATB was remarkable reduced after U87 transfected with shRNA-ATB plasmid （the experimental group） compared with U87 cells transfected with shRNA control （the control group ） . Cloning formation experiment indicated that colony-formation ability was de-creased than that of control group （P 〈0. 01） . MTT assay indicated that the number of viable cell was lower than that of control group （P 〈0. 01） . In addition, Transwell assay further verified that knockdown of ATB significantly inhibited the migration and invasion ability of U87 cells （P 〈0. 01 ） . Conclusion A T B knockdown inhibit glioma cell proliferation, migration and invasion, which indicates that ATB may represent a potential therapeutic target for the treatment of human glioma.