Decreased expression of lncRNA LINC01106 in glioma tissues inhibits proliferation and invasion of glioma cells
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摘要:
目的：分析长链非编码RNA LINC01106在胶质瘤组织以及细胞中的表达水平，探索LINC01106抑制胶质瘤细胞增殖与侵袭能力的潜在作用机制。方法：通过肿瘤基因组图谱（The Cancer Genome Atlas，TCGA）数据库分析LINC01106在胶质瘤中的表达；采用实时荧光定量 PCR（qRT-PCR）法检测胶质瘤细胞系中LINC01106的表达水平。通过转染LINC01106小干扰RNA或者过表达质粒抑制或增高胶质瘤细胞U87中LINC01106的表达水平后，采用 CCK-8实验以及EdU实验检测细胞增殖能力，Transwell实验检测细胞侵袭能力。通过生物信息学以及体外细胞实验对LINC01106潜在的分子机制进行分析。结果：分析TCGA数据库发现LINC01106在胶质瘤肿瘤组织的表达显著降低，同时qRT-PCR结果显示，LINC01106在胶质瘤细胞系（LN229、LN308、U87以及U251）中的表达均显著低于正常对照细胞HEB；体外细胞实验表明，在U87细胞中抑制LINC01106的表达可以显著提高细胞的增殖与侵袭能力，而过表达LINC01106的效果相反。通过生物信息学分析和双荧光素酶报告基因实验发现LINC01106能够结合miR-3167并抑制其表达，而miR-3167可能靶向CBFA2T3，这可能是LINC01106 胶质瘤进展的潜在机制。结论：LINC01106在胶质瘤组织中低表达，抑制LINC01106可促进胶质瘤细胞的增殖与侵袭能力，LINC01106可能通过与CBFA2T3竞争性结合miR-3167在胶质瘤中发挥其抑癌基因的作用。
Abstract:
Objective：To investigate the expression level of LINC01106 in glioma tissues and cell lines and explore the potential mechanism through which LINC01106 affect the proliferation and invasion of glioma cells. Methods：The expression level of LINC01106 in glioma tissues was analyzed by The Cancer Genome Atlas（TCGA）database. QRT-PCR was carried out to detect LINC01106 expression level in glioma tissues and cell lines. The small interfering RNA（siRNA）and overexpressed plasmid（OE）of LINC01106 were applied to suppress or increase the expression level of LINC01106 in U87 cell lines，respectively. CCK-8 assay，EdU assay and transwell assay were performed to assess the effect of LINC01106 on the proliferative and invasive ability of U87 cells. Bioinformatics analysis and in vitro cell experiments were conducted to further explore the potential mechanism of LINC01106. Results：Analysis of the TCGA database revealed that the expression level of LINC01106 was remarkably decreased in glioma tissues. Besides，the results of qRT-PCR showed that the expression levels of LINC01106 in glioma tissues and cell lines were significant lower that in normal controls. Repression of LINC01106 in U87 cells markedly promoted the proliferative and invasive capacities of glioma cells，while overespression of LINC01106 exerted the opposite effects. Bioinformatics analysis and double luciferase reporter gene assay revealed that LINC01106 could bind to miR-3167 and inhibit its expression，while miR-3167 might target CBFA2T3，which might be a potential mechanism for the progression of LINC01106 in glioma. Conclusion：LINC01106 is down-regulated in glioma，and inhibition of LINC01106 can promote the proliferation and invasion of glioma cells. LINC01106 might play its role as a tumor suppressor in gliomas by competitively binding to CBFA2T3 with miR-3167.
