长链非编码RNA loc728196促进胶质瘤发生的调控机制

The regulatory mechanism of long non coding RNA loc728196 in promoting glioma

目的研究长链非编码RNA loc728196促进胶质瘤发生的调控机制。方法通过生物信息学分析和双荧光素酶报告实验发现miR-513c为loc728196下游调控位点,转染miR-513c观察loc728196水平,探讨loc728196与miR-513c之间的关系;对在U251和A172细胞株中miR-513c的目标位点进行搜索,确定miR-513c下游位点TCF7;转染不同干扰RNA后观察U251和A172细胞株增殖、迁移和侵袭情况,通过对比恢复loc728196/miR-513c/TCF7后U251和A172细胞株RNA表达变化情况来验证loc728196对miR-513c/TCF7的调控作用。结果长链非编码RNA loc728196在人脑胶质瘤组织中存在高表达,loc728196敲除可促进U251和A172细胞的miR-513c表达,而转染miR-513c可抑制loc728196水平,沉默loc728196影响胶质瘤细胞的增殖、迁移和侵袭。沉默loc728196抑制了U251和A172细胞中TCF7的表达,而加入miR-513c抑制剂则逆转了这一现象,表明loc728196通过至少部分抑制胶质瘤中miR-513c促进TCF7的表达。结论长链非编码RNA loc728196通过靶向miR一513c/TCF7轴促进胶质瘤的发生。

Objective To discuss the study on the regulation mechanism of LncRNA LOC728196 on glioma growth.Methods Through bioinformatics analysis,the miR-513c,the level of loc728196 were identified and observed by mir-513c transfection and the relationship between loc728196 and mir-513c was discussed;the target of mir-513c in U251 and A172 cell lines was searched.Luciferase analysis showed that mir-513c was bound to tcf7 mRNA at 3'-UTR,and mir-513c target tcf7,the proliferation,migration and invasion of U251 and A172 cell lines were observed by qRT-PCR,and the changes of U251 and A172 cell lines were confirmed by comparing the recovery of loc728196/mir-513c/TCF7.Results Upregulated expression of LOC728196 in glioma,depletion of loc 728196 promoted the expression of mir-513c in U251 and A172 cells,while transfection of mir-513c inhibited the level of loc728196,and silencing loc728196 affected the proliferation,migration and invasion of glioma cells.Conclusion LncRNA LOC728196 facilitates glioma carcinogenesis by targeting/miR-513c/TCF7.