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DGCR5 抑制小儿原发性多形性成胶质细胞瘤的 EMT 并作为预后生物标志物。

DGCR5 suppresses the EMT of pediatric primary glioblastoma multiforme cell and serves as a prognostic biomarker.

机构信息

Department of Pediatrics, Maternal and Child Health, Family Planning Service Center of Shangluo City, Shangluo, Shaan'xi, China.

出版信息

Eur Rev Med Pharmacol Sci. 2019 Nov;23(22):10024-10034. doi: 10.26355/eurrev_201911_19569.

DOI:10.26355/eurrev_201911_19569
PMID:31799672
Abstract

OBJECTIVE

Pediatric primary glioblastoma multiforme (GBM) is a common brain tumor among childhood. Nevertheless, the underlying mechanism of glioblastoma progresses remains to be illuminated. The current study explores the potential functions of long noncoding RNA (lncRNA) DGCR5 in the aggressiveness of GBM.

PATIENTS AND METHODS

The expression of DGCR5 was evaluated by quantitative real-time PCR (qRT-PCR). Immunoblotting was carried out to assess the protein expressions of N-cadherin and E-cadherin. Cell Counting Kit-8 (CCK-8), wound healing, transwell assay, and flow cytometry were applied to explore the roles of DGCR5 in glioblastoma cell malignant biological behaviors.

RESULTS

LncRNA DGCR5 was down expressed in glioblastoma. Transfection of DGCR5 markedly repressed cell viability and colony formation ability of U87 and U251 cells. Additional, DGCR5 overexpression caused cell cycle arrest and increased cell apoptosis. Moreover, upregulation of DGCR5 suppressed the growth and promoted cell apoptosis of U87 cell in vivo. Finally, overexpression of DGCR5 impaired the migration, invasiveness, and reversed epithelial-to-mesenchymal transition (EMT) process of glioblastoma cell.

CONCLUSIONS

LncRNA DGCR5 inhibited the proliferation, aggressiveness phenotypes, and EMT of glioblastoma cell.

摘要

目的

小儿多形性胶质母细胞瘤(GBM)是儿童常见的脑肿瘤。然而,GBM 进展的潜在机制仍有待阐明。本研究探讨了长非编码 RNA(lncRNA)DGCR5 在 GBM 侵袭性中的潜在功能。

患者和方法

通过实时定量 PCR(qRT-PCR)评估 DGCR5 的表达。免疫印迹法评估 N-钙黏蛋白和 E-钙黏蛋白的蛋白表达。细胞计数试剂盒-8(CCK-8)、划痕愈合、Transwell 分析和流式细胞术用于探讨 DGCR5 在神经母细胞瘤细胞恶性生物学行为中的作用。

结果

lncRNA DGCR5 在胶质母细胞瘤中表达下调。DGCR5 的转染显著抑制 U87 和 U251 细胞的细胞活力和集落形成能力。此外,DGCR5 的过表达导致细胞周期停滞并增加细胞凋亡。此外,上调 DGCR5 抑制了 U87 细胞在体内的生长并促进了细胞凋亡。最后,DGCR5 的过表达抑制了神经母细胞瘤细胞的迁移、侵袭能力,并逆转了上皮间质转化(EMT)过程。

结论

lncRNA DGCR5 抑制了神经母细胞瘤细胞的增殖、侵袭表型和 EMT。

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