长链非编码RNA LINC01106在胶质瘤组织中低表达并能够抑制细胞增殖与侵袭

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,对LINC01106抑制胶质瘤细胞增殖与侵袭能力的潜在作用机制进行探索。方法 通过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)的方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U87细胞中LINC01106的表达水平；采用 CCK8实验以及EdU实验对胶质瘤细胞增殖功能进行检测；采用transwell实验检测LINC01106对胶质瘤细胞侵袭功能的影响。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探索。结果 通过分析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的表达可以显著促进细胞的增殖与侵袭能力,而过表达LINC01106则有着相反的效果。LINC01106能够结合miR-3167并抑制其表达,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可能通过结合miR-3167在胶质瘤中发挥其抑癌基因的作用。

Long noncoding RNA LINC01106 expression level is decreased in glioma tissues and it inhibits proliferation and invasion of glioma cells

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 LINC01106 expression in glioma tissues was analyzed by The Cancer Genome Atlas (TCGA) database. QRT-PCR was carried out to examine LINC01106 expression levels in glioma cell lines. The small interfering RNA (siRNA) and overexpressed plasmid (OE) of LINC01106 were used to suppress or increase the expression level of LINC01106 in U87 cell lines, respectively. CCK8, EdU and transwell assays 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 LINC01554 action using Results Analysis of the TCGA database revealed that LINC01106 was remarkably underexpressed in glioma tissues. Besides, the results of qRT-PCR showed that the expression level of LINC01106 in glioma cell lines was significant lower that in human normal glial cell line HEB. Repression of LINC01106 in U87 cells markedly promoted the proliferative and invasive capacities of glioma cells, while LINC01106 overespression exerted the opposite effects. LINC01106 could bind miR-3167, thereby providing possible mechanisms by whichthereby providing possible mechanisms by which LINC01554 could participate in the progression of glioma. Conclusions LINC01106 is down-regulated in glioma, and inhibition of LINC01106 can promote the proliferation and invasion of glioma cells. LINC01106 may bind to miR-3167 and exert its anti-cancer effect in glioma.