[1]王壮壮,刘彦廷,龚伟,等.沉默lncRNA MALAT1表达对胶质瘤细胞增殖和凋亡的影响[J].中国临床神经外科杂志,2023,28(06):390-394.[doi:10.13798/j.issn.1009-153X.2023.06.011]
　WANG Zhuang-zhuang,LIU Yan-ting,GONG Wei,et al.Effect of silencing lncRNA MALAT1 expression on proliferation and apoptosis of glioma cells[J].,2023,28(06):390-394.[doi:10.13798/j.issn.1009-153X.2023.06.011]
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沉默lncRNA MALAT1表达对胶质瘤细胞增殖和凋亡的影响()
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《中国临床神经外科杂志》[ISSN:1009-153X/CN:42-1603/TN]

卷:
28
期数:
2023年06期
页码:
390-394
栏目:
实验研究
出版日期:
2023-06-30

文章信息/Info

Title:
Effect of silencing lncRNA MALAT1 expression on proliferation and apoptosis of glioma cells
文章编号:
1009-153X（2023）06-0390-05
作者:
王壮壮; 刘彦廷; 龚伟; 周猛; 贾文学; 艾文兵; 田春雷
443003湖北宜昌，三峡大学第一临床医学院（宜昌市中心人民医院）神经外科（王壮壮、刘彦廷、龚伟、周猛、贾文学、田春雷）；443003湖北，宜昌市夷陵医院神经外科（艾文兵）
Author(s):
WANG Zhuang-zhuang1;  LIU Yan-ting1;  GONG Wei1;  ZHOU Meng1;  JIA Wen-xue1;  AI Wen-bing2;  TIAN Chun-lei1
1. Department of Neurosurgery, The First Clinical Medical College of China Three Gorges University (Yichang Central People’s Hospital), Yichang 443003, China; 2. Department of Neurosurgery, Yiling Hospital of Yichang City, Yichang 443003, China
关键词:
胶质瘤; 长链非编码RNA MALAT1; 细胞增殖; 细胞凋亡
Keywords:
Glioma;  U87 cell;  A172 cell;  Long non-coding RNA MALAT1;  Cell proliferation;  Cell apoptosis
分类号:
A
DOI:
10.13798/j.issn.1009-153X.2023.06.011
文献标志码:
R 739.41
摘要:
目的 探讨沉默lncRNA MALAT1表达对胶质瘤细胞增殖和凋亡的影响。方法 从CGGA数据库下载胶质瘤lncRNA MALAT1表达谱数据，采用生信方法分析胶质瘤组织lncRNA MALAT1的表达。体外培养U87、A172，转染lncRNA MALAT1质粒沉默其表达（sh-MALAT1组），以转染空白质粒为对照（sh-NC组）；使用CCK-8法和流式细胞术检测胶质瘤细胞增殖和凋亡；TargetScan软件预测lncRNA MALAT1靶蛋白并使用免疫印迹法检测U87、A172细胞相关蛋白表达。结果 生信分析显示，胶质瘤lncRNA MALAT1表达量明显高于正常组织（P<0.05），而且lncRNA MALAT1高表达胶质瘤病人总生存期明显缩短（P<0.05）。sh-MALAT1组U87和A172细胞增殖活性均明显低于sh-NC组（P<0.05），而细胞凋亡率明显高于sh-NC组（P<0.01）。TargetScan软件分析显示STMN1、RAB5A和ATG4D蛋白为lncRNA MALAT1的下游靶点，免疫印迹法检测显示sh-MALAT1组U87和A172细胞STMN1、RAB5A和ATG4D蛋白表达量明显高于sh-NC组（P<0.05）。结论 胶质瘤lncRNA MALAT1呈高表达，可能通过靶向上调STMN1、RAB5A和ATG4D蛋白的表达水平，促进胶质瘤细胞增殖、抑制胶质瘤细胞凋亡。沉默lncRNA MALAT1表达明显抑制胶质瘤细胞增殖、促进其凋亡。
Abstract:
Objective To investigate the effect of silencing lncRNA MALAT1 expression on the proliferation and apoptosis of glioma cells. Methods The lncRNA MALAT1 expression data were downloaded from CGGA database, and the expression of lncRNA MALAT1 in glioma tissues was analyzed by bioinformatics method. U87 and A172 were cultured in vitro, and those transfected with lncRNA MALAT1 plasmid to silence their expression were served as sh-MALAT1 group, and those transfected with blank plasmid were served as control (sh-NC group). The proliferation and the apoptosis of glioma cells were detected by CCK-8 method and flow cytometry, respectively. The lncRNA MALAT1 target protein was predicted by TargetScan software and associated protein expression in U87 and A172 cells was detected by western blotting. Results Bioinformatics analysis showed that lncRNA MALAT1 expression in glioma tissues was significantly higher than that in normal tissues (P<0.05), and the overall survival of glioma patients with high lncRNA MALAT1 expression was significantly shortened (P<0.05). The proliferative activities of U87 and A172 cells in sh-MALAT1 group were significantly lower than those in sh-NC group (P<0.05), and the apoptosis rates were significantly higher than those in sh-NC group (P<0.01). TargetScan software analysis showed that STMN1, RAB5A and ATG4D proteins were the downstream targets of lncRNA MALAT1. Western blotting showed that the protein expressions of STMN1, RAB5A and ATG4D in U87 and A172 cells in sh-MALAT1 group were significantly higher than those in sh-NC group (P<0.05). Conclusions The lncRNA MALAT1 is highly expressed in glioma, which may promote the proliferation of glioma cells and inhibit the apoptosis of glioma cells through targeted up-regulation of STMN1, RAB5A and ATG4D proteins. Silencing lncRNA MALAT1 expression significantly inhibited the proliferation of glioma cells and promoted their apoptosis.

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备注/Memo

备注/Memo:
（2022-07-19收稿，2023-04-30修回）
基金项目：国家自然科学基金（81701278）；湖北省卫健委项目（WJ2019M063）；宜昌市卫生医疗科技项目（A18-301-03）
通讯作者：田春雷，E-mail：cltianyc@163.com
艾文兵，E-mail：1043642574@qq.com
更新日期/Last Update: 2022-06-30