LINC00152 acts as a potential marker in gliomas and promotes tumor proliferation and invasion through the LINC00152/miR-107/RAB10 axis,Journal of Neuro-Oncology

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LINC00152 acts as a potential marker in gliomas and promotes tumor proliferation and invasion through the LINC00152/miR-107/RAB10 axis
Journal of Neuro-Oncology ( IF 3.2 ) Pub Date : 2021-09-03 , DOI: 10.1007/s11060-021-03836-1
Gang Peng ₁ , Jun Su ₁ , Songhua Xiao ₂ , Qing Liu _{1,

3}

Affiliation

Purpose

Aberrant expression of long noncoding RNAs plays a pivotal role in tumorigenesis. Recently, several studies have showed that the LINC00152 gene is upregulated in a variety of tumors and plays an oncogene role; however, its underlying molecular mechanisms in glioblastoma remain unclear. In this study, we prepare to investigate the biological role and underlying molecular mechanisms of LINC00152 in glioblastoma cells.

Methods

Bioinformatics analysis to identify LINC00152 expression, Cell Counting kit-8 assay and Colony formation assay were used to evaluate proliferation, Flow cytometric analysis was used to evaluate apoptosis, Cell Matrigel invasion assay and Wound healing assay was used to evaluate invasion, Western blot analysis to check protein expression level, Mouse xenograft models was used to check cell proliferation in vivo.

Results

In this study, we found that LINC00152 was upregulated in gliomas and its expression was significantly associated with high tumor aggressiveness and poor outcomes for glioma patients. Functionally, the knockdown of LINC00152 not only inhibited malignant behaviors of glioma, such as proliferation and invasion of glioma cells and induced apoptosis in vitro but also suppressed tumorigenesis in vivo. Mechanistically, results of the bioinformatics analysis and experimental studies confirmed that LINC00152 and RAB10 as the targets of miR-107, and LINC00152 might act as a sponge for miR-107 to regulate the expression of RAB10 in glioblastoma. Additionally, silencing miR-107 reversed the effects induced by LINC00152 knockdown on glioblastoma cells both in vitro and in vivo.

Conclusion

Our data suggested that LINC00152 is a candidate prognostic marker of glioma, and that the LINC00152/MIR-107/RAB10 axis plays a pivotal role in regulation of the glioma malignancy, and therefore, targeting the axis might be an effective therapeutic strategy to treat glioma.

Graphic abstract

中文翻译：

LINC00152 作为胶质瘤的潜在标志物，通过 LINC00152/miR-107/RAB10 轴促进肿瘤增殖和侵袭

目的

长链非编码 RNA 的异常表达在肿瘤发生中起关键作用。最近，多项研究表明LINC00152基因在多种肿瘤中上调并发挥癌基因作用；然而，其在胶质母细胞瘤中的潜在分子机制仍不清楚。在这项研究中，我们准备研究 LINC00152 在胶质母细胞瘤细胞中的生物学作用和潜在的分子机制。

方法

生物信息学分析鉴定LINC00152表达，细胞计数试剂盒8测定和集落形成测定用于评估增殖，流式细胞术分析用于评估细胞凋亡，细胞基质胶侵袭测定和伤口愈合测定用于评估侵袭，蛋白质印迹分析用于检查蛋白质表达水平，小鼠异种移植模型用于检查体内细胞增殖。

结果

在这项研究中，我们发现 LINC00152 在胶质瘤中上调，其表达与胶质瘤患者的高肿瘤侵袭性和不良预后显着相关。在功能上，LINC00152的敲低不仅抑制了胶质瘤的恶性行为，如胶质瘤细胞的增殖和侵袭，并在体外诱导细胞凋亡，而且在体内抑制了肿瘤的发生。机制上，生物信息学分析和实验研究结果证实LINC00152和RAB10作为miR-107的靶标，LINC00152可能作为miR-107的海绵调节胶质母细胞瘤中RAB10的表达。此外，沉默 miR-107 在体外和体内逆转了 LINC00152 敲低对胶质母细胞瘤细胞的影响。