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长非编码 RNA MIAT 通过海绵吸附 miR-1246 促进非小细胞肺癌进展。

Long non-coding RNA MIAT promotes non-small cell lung cancer progression by sponging miR-1246.

机构信息

Department of Thoracic Oncology, Fujian Cancer Hospital & Fujian Medical University Cancer Hospital, Fuzhou, Chin.

出版信息

Eur Rev Med Pharmacol Sci. 2019 Jul;23(13):5795-5801. doi: 10.26355/eurrev_201907_18318.

Abstract

OBJECTIVE

Recently, long non-coding ribonucleic acids (lncRNAs) have attracted more attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA MIAT in the progression of non-small cell lung cancer (NSCLC) and to explore the possible underlying mechanism.

PATIENTS AND METHODS

MIAT expression in NSCLC tissue samples was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The association between the expression of MIAT and the prognosis of NSCLC patients were explored. Furthermore, the wound healing assay and the transwell assay were conducted in vitro. In addition, the luciferase assay and the RNA immunoprecipitation assay (RIP) were used to elucidate the underlying mechanism.

RESULTS

The MIAT expression in NSCLC tissues was significantly higher than that of the corresponding normal tissues. Meanwhile, the MIAT expression was associated with the overall survival time of NSCLC patients. The migration and invasion of cells were significantly promoted after MIAT was over-expressed in vitro. Meanwhile, the cell migration and cell invasion were obviously remarkedly inhibited after MIAT knock-down in vitro. Bioinformatics analysis predicted that microRNA-1246 (miR-1246) was as a novel target for MIAT. The expression of miR-1246 was significantly down-regulated or up-regulated after the overexpression or down-expression of MIAT, respectively. Further mechanism assays showed that miR-1246 was a direct target of MIAT in NSCLC.

CONCLUSIONS

MIAT enhanced the NSCLC cell migration and invasion via targeting miR-1246, which might be a potential biomarker in NSCLC.

摘要

目的

长链非编码核糖核酸(lncRNA)在肿瘤进展中的作用引起了越来越多的关注。本研究旨在探讨 lncRNA MIAT 在非小细胞肺癌(NSCLC)进展中的确切作用,并探讨其可能的潜在机制。

患者和方法

通过实时定量聚合酶链反应(qRT-PCR)检测 NSCLC 组织样本中的 MIAT 表达。探讨 MIAT 表达与 NSCLC 患者预后的关系。此外,还进行了体外划痕愈合试验和 Transwell 试验。此外,还使用了荧光素酶报告基因检测和 RNA 免疫沉淀(RIP)实验来阐明潜在机制。

结果

MIAT 在 NSCLC 组织中的表达明显高于相应的正常组织。同时,MIAT 的表达与 NSCLC 患者的总生存时间有关。体外过表达 MIAT 后,细胞的迁移和侵袭明显增强。同时,体外敲低 MIAT 后,细胞迁移和细胞侵袭明显受到抑制。生物信息学分析预测 microRNA-1246(miR-1246)是 MIAT 的一个新的靶标。MIAT 的过表达或下调分别导致 miR-1246 的表达明显下调或上调。进一步的机制研究表明,miR-1246 是 NSCLC 中 MIAT 的直接靶标。

结论

MIAT 通过靶向 miR-1246 增强 NSCLC 细胞的迁移和侵袭,可能是 NSCLC 的潜在生物标志物。

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