Suppr超能文献

长链非编码 RNA 00707 海绵 microRNA-613(miR-613)促进神经胶质瘤的增殖和侵袭。

The Long Intergenic Noncoding RNA 00707 Sponges MicroRNA-613 (miR-613) to Promote Proliferation and Invasion of Gliomas.

机构信息

Department of Neurosurgery, Xiangyang Center Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China.

出版信息

Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820962092. doi: 10.1177/1533033820962092.

Abstract

BACKGROUND

Glioma is one of the most deadly malignant tumors in humans. Long non-coding RNA (lncRNA) plays a key role in the occurrence, development and invasion of tumors by regulating oncogenic and tumor suppressor pathways. However, the role and action mechanism of long intergenic non-coding RNA 00707 (LINC00707) in gliomas have not been elucidated. This study aimed to investigate the interaction between LINC00707 and miR-613 as well as its role in gliomas.

MATERIALS AND METHODS

The expression levels of LINC00707 and miR-613 were detected by qRT-PCR. The chi-square test was used to analyze the correlation between LINC00707 expression and clinicopathological parameters. CCK-8 and colony formation assays were used to detect glioma cell proliferation; and wound healing and transwell assays were used to detect glioma cell migration and invasion. The relationship between LINC00707 and miR-613 was predicted by Starbase, and verified by qRT-PCR and dual luciferase reporter gene assay.

RESULTS

LINC00707 was up-regulated in gliomas. Up-regulated LINC00707 increased the proliferation, migration and invasion of glioma cells, and silenced LINC00707 reduced these abilities. The increase of the expression level of LINC00707 down-regulated miR-613 in glioma cells, while the inhibition of the expression level of LINC00707 up-regulated miR-613 in glioma cells. The high expression of LINC00707 was related to the Karnofsky performance status (KPS) score and WHO staging. LINC00707 could offset the ability of miR-613 to inhibit glioma proliferation and invasion.

CONCLUSION

LINC00707 promotes proliferation and invasion of glioma cells by sponging miR-613. The regulatory axis of LINC00707/miR-613 provides new insights into the mechanism and treatment of gliomas.

摘要

背景

神经胶质瘤是人类最致命的恶性肿瘤之一。长链非编码 RNA(lncRNA)通过调节致癌和肿瘤抑制途径在肿瘤的发生、发展和侵袭中发挥关键作用。然而,长链非编码 RNA 00707(LINC00707)在神经胶质瘤中的作用和作用机制尚不清楚。本研究旨在探讨 LINC00707 与 miR-613 的相互作用及其在神经胶质瘤中的作用。

材料和方法

通过 qRT-PCR 检测 LINC00707 和 miR-613 的表达水平。采用卡方检验分析 LINC00707 表达与临床病理参数的相关性。CCK-8 和集落形成实验用于检测神经胶质瘤细胞增殖;划痕愈合和 Transwell 实验用于检测神经胶质瘤细胞迁移和侵袭。通过 Starbase 预测 LINC00707 和 miR-613 之间的关系,并通过 qRT-PCR 和双荧光素酶报告基因实验进行验证。

结果

LINC00707 在神经胶质瘤中上调。上调 LINC00707 增加了神经胶质瘤细胞的增殖、迁移和侵袭能力,而沉默 LINC00707 则降低了这些能力。LINC00707 在神经胶质瘤细胞中的表达水平增加导致 miR-613 下调,而 LINC00707 表达水平的抑制导致 miR-613 上调。LINC00707 的高表达与卡氏功能状态(KPS)评分和世界卫生组织(WHO)分期有关。LINC00707 可以抵消 miR-613 抑制神经胶质瘤增殖和侵袭的能力。

结论

LINC00707 通过海绵吸附 miR-613 促进神经胶质瘤细胞的增殖和侵袭。LINC00707/miR-613 的调控轴为神经胶质瘤的发生机制和治疗提供了新的见解。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验