摘要
目的探讨长链非编码(lncRNA)SNORD3A在胶质瘤组织和胶质瘤细胞系中的表达变化,以及对胶质瘤细胞增殖和侵袭能力的影响。方法采用生物信息学方法分析美国国家生物技术信息中心(NCBI)GEO数据库收录的GSE58276中差异表达的lncRNA,采集2017年6月至2019年8月手术切除的胶质瘤组织标本30例,实时荧光定量聚合酶链反应(PCR)检测lncRNA SNORD3A表达水平;小干扰RNA转染胶质瘤细胞系T98G和U251,CCK⁃8细胞增殖实验检测胶质瘤细胞增殖能力、Transwell细胞侵袭实验检测胶质瘤细胞侵袭能力、Western blotting法检测胶质瘤细胞c⁃Myc mRNA和蛋白表达变化。结果与对照组相比,胶质瘤组织lncRNA SNORD3A表达水平升高(P=0.000);与HEB细胞相比,胶质瘤细胞系T98G、U87、U251和U373 lncRNA SNORD3A表达升高(均P<0.05)。si⁃SNORD3A⁃1组和si⁃SNORD3A⁃2组T98G细胞(P=0.001,0.007)和U251细胞(P=0.002,0.009)lncRNA SNORD3A表达水平低于对照组;转染后24、48和72 h,si⁃SNORD3A⁃1组和si⁃SNORD3A⁃2组T98G细胞(均P=0.000)和U251细胞(均P=0.000)增殖能力低于对照组;转染后48 h,si⁃SNORD3A⁃1组和si⁃SNORD3A⁃2组穿过小室的T98G和U251细胞数目少于对照组(均P=0.000)、c⁃Myc mRNA和蛋白表达水平低于对照组(均P<0.01)。结论lncRNA SNORD3A可能通过靶向c⁃Myc蛋白促进T98G和U251细胞的增殖和侵袭。
Objective To explore the expression of long non⁃coding RNA (lncRNA) SNORD3A inglioma tissues and cell lines and its effect on proliferation and invasion of glioma cells. Methods Weanalyzed the differentially expressed lncRNAs in the National Center for Biotechnology Information (NCBI)GEO (GSE58276) by bioinformatics. A total of 30 glioma tissue specimen were collected from June 2017 toAugust 2019, lncRNA SNORD3A expression was detected by real⁃time fluorescence quantitative polymerasechain reaction (PCR). The si⁃SNORD3A was transfected into T98G and U251 cells. CCK⁃8 was used toanalyze the proliferative capacity of cells. Transwell assay was used to detect cell invasion changes. Theexpression of c⁃Myc protein was detected by Western blotting. Results Compared with the control group,the expression level of lncRNA SNORD3A in glioma tissue was increased (P = 0.000). Compared with HEBcells, the expression levels of T98G, U87, U251 and U373 lncRNA SNORD3A in glioma cell lines wereelevated (P < 0.05, for all). The expression levels of lncRNA SNORD3A in T98G cells (P = 0.001, 0.007)and U251 cells (P = 0.002, 0.009) in si⁃SNORD3A⁃1 group and si⁃SNORD3A⁃2 group were lower than thosein control group. At 24, 48 and 72 h after transfection, the proliferation capacity of T98G cells (P = 0.000,for all) and U251 cells (P = 0.000, for all) in si⁃SNORD3A⁃1 and si⁃SNORD3A⁃2 groups were lower thanthose in control group. At 48 h after transfection, the number of T98G and U251 cells passing through the chamber in si⁃SNORD3A⁃1 and si⁃SNORD3A⁃2 groups were less than those in control group (P = 0.000, forall), and the levels of c⁃Myc mRNA and protein expression were lower than control group (P < 0.01, for all). Conclusions lncRNA SNORD3A promotes proliferation and invasion of T98G and U251 cells by partlytargeting c⁃Myc.
作者
慕茂林
牛万祥
张晓明
汤深凤
胡珊珊
牛朝诗
MU Mao⁃lin;NIU Wan⁃xiang;ZHANG Xiao⁃ming;TANG Shen⁃feng;HU Shan⁃shan;NIU Chao⁃shi(Department of Neurosurgery,Anhui Provincial Hospital Affiliated to Anhui Medical University,Anhui Province Key Laboratory of Brain Function and Brain Disease,Hefei 230001,Anhui,China)
出处
《中国现代神经疾病杂志》
CAS
北大核心
2019年第12期945-953,共9页
Chinese Journal of Contemporary Neurology and Neurosurgery
基金
脑功能与脑疾病安徽省重点实验室绩效考核补助项目(项目编号:1606c08235)
中央引导地方科技发展专项项目(项目编号:2017070802D144)
安徽省自然科学基金青年科学基金资助项目(项目编号:1908085QH336)~~