Department of Neurosurgery, Xiangyang Center Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, China.
Technol Cancer Res Treat. 2020 Jan-Dec;19:1533033820962092. doi: 10.1177/1533033820962092.
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.
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.
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.
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.
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。
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。
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。
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。
