Long Non-coding RNA PVT1 Competitively Binds MicroRNA-424-5p to Regulate CARM1 in Radiosensitivity of Non-Small-Cell Lung Cancer (Retracted article. See vol. 28, pg. 755, 2022)
Long Non-coding RNA PVT1 Competitively Binds MicroRNA-424-5p to Regulate CARM1 in Radiosensitivity of Non-Small-Cell Lung Cancer (Retracted article. See vol. 28, pg. 755, 2022)
复制标题
长非编码RNA PVT1 竞争性结合MicroRNA-424-5p 调节CARM1 在非小细胞肺癌放射敏感性中的作用
DOI：
10.1016/j.omtn.2018.12.006
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发表时间：
2019-06-07
影响因子：
8.8
通讯作者：
Hu, Yi
中科院分区：
文献类型：
--
作者：
Wang, Dong;Hu, Yi
越来越多的证据表明，长链非编码RNA（IncRNA）表达异常参与肿瘤的发生和发展。本研究旨在探讨lncRNA PVT 1通过microRNA（miR）-424-5p/lncRNA PVT 1/CARM 1信号通路对非小细胞肺癌（NSCLC）放射敏感性的影响。筛选差异表达的IncRNA。预测lncRNA共表达基因，并进行基因本体分析，寻找与NSCLC放射敏感性相关的基因。筛选与IncRNA和mRNA结合的miR。选择两种具有最高表达的PVT 1的细胞系，然后用一系列不同的模拟物、抑制剂或siRNA转染。采用RIP法检测PVT 1与CARM 1的相互作用。研究了miR-424- 5 p对细胞增殖、迁移、侵袭、周期和凋亡的调节作用。PVT 1是NSCLC中上调最显著的lncRNA。CARM 1与lncRNA PVT 1共表达，与NSCLC放射敏感性相关。IncRNA PVT 1和CARM 1均能与miR-424- 5 p联合收割机结合。在NSCLC组织中发现PVT 1、CARM 1、MMP-2、MMP-9和Bcl-2增加，而miR-424- 5 p和Bax减少。PVT 1被miR-424- 5 p靶向。在沉默PVT 1或过表达miR-424- 5 p后，减少PVT 1、CARM 1、MMP-2、MMP-9和Bcl-2抑制细胞增殖、迁移和侵袭，但促进miR-424- 5 p、Bax和细胞凋亡。本研究证实siRNA-PVT 1和过表达的miR-424- 5 p可以增加NSCLC放射治疗的放射敏感性。
Accumulating evidence revealed that dysregulated long non-coding RNAs (IncRNAs) were involved in tumorigenesis and progression. This study is supposed to reveal the effects of lncRNA PVT1 on the radiosensitivity of non-small-cell lung cancer (NSCLC) via the microRNA (miR)-424-5p/IncRNA PVT1/CARM1 signaling pathway. Differentially expressed IncRNA was filtrated. The co-expressed gene of lncRNA was predicted, and gene ontology analysis was performed to find out the genes associated with NSCLC radiosensitivity. The miR that was combined with IncRNA and mRNA was filtrated. Two cell lines with the highest expressed PVT1 were selected, followed by transfection with a series of different mimic, inhibitor, or siRNA. RIP assay was employed for the interaction between PVT1 and CARM1. The regulatory effect of miR-424-5p on cell proliferation, migration, invasion, cycle, and apoptosis was investigated. PVT1 was the most remarkable lncRNA that upregulated in NSCLC. CARM1 co-expressed with lncRNA PVT1 and associated with NSCLC radiosensitivity. Both IncRNA PVT1 and CARM1 can combine with miR-424-5p. Increased PVT1, CARM1, MMP-2, MMP-9, and Bcl-2 and decreased miR-424-5p and Bax were found in NSCLC tissues. PVT1 was targeted by miR-424-5p. After silencing of PVT1 or overexpressed miR-424-5p, decreased PVT1, CARM1, MMP-2, MMP-9, and Bcl-2 inhibited cell proliferation, migration, and invasion but promoted miR-424-5p, Bax, and cell apoptosis. The present study confirms the radiosensitivity of NSCLC radiotherapy can be increased by siRNA-PVT1 and overexpressed miR-424-5p.