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长链非编码RNA MRPL39通过调控非小细胞肺癌中的miR-130/TSC1轴抑制细胞增殖和迁移。

LncRNA MRPL39 inhibits cell proliferation and migration by regulating miR-130/TSC1 axis in non-small cell lung cancer.

作者信息

Fan Qinghao, Bao Xianrong, Zhao Han, Li Sichen

机构信息

Cardiothoracic Surgery, Jinhua People's Hospital, Jinhua, 321000 China.

出版信息

3 Biotech. 2024 May;14(5):125. doi: 10.1007/s13205-024-03975-y. Epub 2024 Apr 2.

DOI:10.1007/s13205-024-03975-y
PMID:38577417
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10987421/
Abstract

Currently, the effect of miR-130 on non-small cell lung cancer (NSCLC) remains controversial. In this study, the expression of miR-130 and lncRNA MRPL39 in tumor and non-tumor tissues of NSCLC patients was examined using real-time PCR (RT-PCR) and correlated with the prognosis of NSCLC. The phenotypic effects of miR-130 and MRPL39 on proliferation and migration of NSCLC cell line A549 cells were assessed through CCK-8 and Transwell assays with miR-130 mimic and MRPL39 (mitochondrial ribosomal protein L39) overexpressed plasmid transfection. StarBase/TargetScan analysis and dual-luciferase reporter gene assays were conducted to investigate the relationship between MRPL39, miR-130, and Tuberculosis sclerosis 1 (TSC1). MiR-130 was overexpressed, and MRPL39 was downregulated in NSCLC tissues and cells. Inhibition of miR-130 expression and overexpression of MRPL39 resulted in the inhibition of the viability and migration of A549 cells. MRPL39 is a potential upstream regulatory long non-coding RNA of miR-130, and its expression is negatively regulated by miR-130. TSC1 was identified as a target of miR-130, suppressing the antitumor effects of FGD5-AS1 silencing on GBM cells. After overexpression of MRPL39, the mRNA and protein levels of TSC1 in A549 cells significantly increased. However, after transfection with miR-130 mimic, the up-regulation of mRNA and protein was inhibited, leading to the suppression of cell proliferation and migration.

摘要

目前,miR-130对非小细胞肺癌(NSCLC)的影响仍存在争议。在本研究中,采用实时荧光定量聚合酶链反应(RT-PCR)检测了NSCLC患者肿瘤组织和非肿瘤组织中miR-130和长链非编码RNA MRPL39的表达,并将其与NSCLC的预后相关联。通过CCK-8法和Transwell实验,利用miR-130模拟物和过表达MRPL39(线粒体核糖体蛋白L39)的质粒转染,评估了miR-130和MRPL39对NSCLC细胞系A549细胞增殖和迁移的表型效应。进行了StarBase/TargetScan分析和双荧光素酶报告基因实验,以研究MRPL39、miR-130和结节性硬化症1(TSC1)之间的关系。在NSCLC组织和细胞中,miR-130过表达,而MRPL39表达下调。抑制miR-130表达和过表达MRPL39可导致A549细胞活力和迁移受到抑制。MRPL39是miR-130潜在的上游调控长链非编码RNA,其表达受到miR-130的负调控。TSC1被鉴定为miR-130的靶标,抑制了FGD5-AS1沉默对胶质母细胞瘤细胞的抗肿瘤作用。过表达MRPL39后,A549细胞中TSC1的mRNA和蛋白水平显著升高。然而,用miR-130模拟物转染后,mRNA和蛋白的上调受到抑制,导致细胞增殖和迁移受到抑制。

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本文引用的文献

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miR-375 Combined with SHOX2 Methylation has Higher Diagnostic Efficacy for Non-Small-Cell Lung Cancer.miR-375 联合 SHOX2 甲基化对非小细胞肺癌具有更高的诊断效能。
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LncRNA SOX2-OT/miR-30d-5p/PDK1 Regulates PD-L1 Checkpoint Through the mTOR Signaling Pathway to Promote Non-small Cell Lung Cancer Progression and Immune Escape.长链非编码RNA SOX2-OT/微小RNA-30d-5p/丙酮酸脱氢酶激酶1通过mTOR信号通路调节程序性死亡受体配体1检查点,以促进非小细胞肺癌进展和免疫逃逸。
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circSNX6 (hsa_circ_0031608) enhances drug resistance of non-small cell lung cancer (NSCLC) via miR-137.circSNX6 (hsa_circ_0031608) 通过 miR-137 增强非小细胞肺癌(NSCLC)的耐药性。
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