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LINC00702通过调控miR-510/PTEN轴抑制非小细胞肺癌的增殖和侵袭。

LINC00702 suppresses proliferation and invasion in non-small cell lung cancer through regulating miR-510/PTEN axis.

作者信息

Yu Wencheng, Li Daowei, Ding Xiaoyan, Sun Yong, Liu Yanli, Cong Jinpeng, Yang Jiong, Sun Jian, Ning Xuchao, Wang Hongmei, Xu Tao

机构信息

Department of Respiratory, the Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.

Department of Respiratory, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, China.

出版信息

Aging (Albany NY). 2019 Mar 6;11(5):1471-1485. doi: 10.18632/aging.101846.

DOI:10.18632/aging.101846
PMID:30840927
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6428098/
Abstract

BACKGROUND

Long non-coding RNAs (lncRNAs) have been consistently reported to be involved in the progression of non-small cell lung cancer (NSCLC). In this study, we aimed to identify aberrantly expressed lncRNAs in NSCLC, in order to explore new therapeutic targets for NSCLC.

METHODS

Two pairs of NSCLC and adjacent normal tissues were first analyzed by RNA sequencing. The expressions of LINC00702 in 40 pairs patient samples and in 4 NSCLC cell lines was measured by quantitative real-time PCR. Putative target miRNAs of LINC00702 were predicted by the bioinformatics tools. The effect of LINC00702 on tumor growth was evaluated.

RESULTS

LINC00702 was significantly down-regulated in patients with NSCLC, which was correlated with tumor size and metastasis. In addition, overexpression of LINC00702 markedly suppressed proliferation and metastasis in NSCLC cells via inducing apoptosis and . Moreover, bioinformatics and luciferase reporter assays demonstrated that LINC00702 functioned as a competing endogenous RNA (ceRNA) for miR-510 in NSCLC, and upregulated its target gene PTEN.

CONCLUSION

Our results indicated that LINC00702 modulated the expression of PTEN gene by acting as a ceRNA for miR-510 in NSCLC. Therefore, LINC00702 may serve as a potential target for the diagnosis and treatment of patients with NSCLC.

摘要

背景

长期以来，一直有报道称长链非编码RNA（lncRNAs）参与非小细胞肺癌（NSCLC）的进展。在本研究中，我们旨在鉴定NSCLC中异常表达的lncRNAs，以探索NSCLC的新治疗靶点。

方法

首先通过RNA测序分析两对NSCLC组织及其相邻正常组织。通过定量实时PCR检测40对患者样本和4种NSCLC细胞系中LINC00702的表达。利用生物信息学工具预测LINC00702的潜在靶标miRNA。评估LINC00702对肿瘤生长的影响。

结果

LINC00702在NSCLC患者中显著下调，这与肿瘤大小和转移相关。此外，LINC00702的过表达通过诱导凋亡显著抑制NSCLC细胞的增殖和转移。此外，生物信息学和荧光素酶报告基因检测表明，LINC00702在NSCLC中作为miR-510的竞争性内源RNA（ceRNA）发挥作用，并上调其靶基因PTEN。

结论

我们的结果表明，LINC00702在NSCLC中作为miR-510的ceRNA调节PTEN基因的表达。因此，LINC00702可能作为NSCLC患者诊断和治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/b04b7f5b60a5/aging-11-101846-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/6c5af148bd5b/aging-11-101846-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/fffa311795b7/aging-11-101846-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/5d73833f1c2b/aging-11-101846-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/7d2bd325c486/aging-11-101846-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/eba25d185f30/aging-11-101846-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/634bf20c2ec0/aging-11-101846-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/3154317f1eb9/aging-11-101846-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/b04b7f5b60a5/aging-11-101846-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/6c5af148bd5b/aging-11-101846-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/fffa311795b7/aging-11-101846-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/5d73833f1c2b/aging-11-101846-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/7d2bd325c486/aging-11-101846-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/eba25d185f30/aging-11-101846-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/634bf20c2ec0/aging-11-101846-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/3154317f1eb9/aging-11-101846-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1201/6428098/b04b7f5b60a5/aging-11-101846-g008.jpg

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