Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expressionReportar como inadecuado




Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Molecular Cancer

, 16:17

First Online: 21 January 2017Received: 13 August 2016Accepted: 03 January 2017DOI: 10.1186-s12943-017-0581-3

Cite this article as: Chen, Q., Chen, X., Chen, Z. et al. Mol Cancer 2017 16: 17. doi:10.1186-s12943-017-0581-3

Abstract

BackgroundNumerous studies have shown that long non-coding RNAs lncRNAs behave as a novel class of transcript during multiple cancer processes, such as cell proliferation, apoptosis, migration, and invasion. LINC00152 is located on chromosome 2p11.2, and has a transcript length of 828 nucleotides. The biological role of LINC00152 in LADlung adenocarcinoma remains unknown.

MethodsQuantitative reverse transcription PCRqRT-PCR was used to detect LINC00152 expression in 60 human LAD tissues and paired normal tissues. In vitro and in vivo studies showed the biological function of LINC00152 in tumour progression. RNA transcriptome sequencing technology was performed to identify the downstream suppressor IL24interleukin 24 which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation RIP, RNA pulldown, and Chromatin immunoprecipitation ChIP assays were carried out to reveal the interaction between LINC00152, EZH2 and IL24.

ResultsLINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. High levels of LINC00152 expression were correlated with advanced TNM stage, larger tumor size, and lymph node metastasis, as well as shorter survival time. Silencing of LINC00152 suppressed cell growth and induced cell apoptosis. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. Moreover, the ectopic expression of IL24 repressed cell proliferation and partly reversed LINC00152 overexpression-induced promotion of cell growth in LAD.

ConclusionsOur study reveals an oncogenic role for LINC00152 in LAD tumorigenesis, suggesting that it could be used as a therapeutic target in LAD treatment.

KeywordsLong intergenic non-coding RNA LINC00152 Lung adenocarcinoma Proliferation IL24 AbbreviationsChIPChromatin immunoprecipitation

EZH2Enhancer of zeste homolog 2

H3K27me3Histone H3 lysine 27 trimethylation

HCCHepatocellular carcinoma

IL24Interleukin 24

LADLung adenocarcinoma

LINC00152Long intergenic non-coding RNA 00152

lncRNAsLong noncoding RNAs

MDA-7Melanoma differentiation-associated gene-7

miRNAsMicroRNAs

NSCLCNon-small cell lung cancer

qRT-PCRQuantitative reverse transcriptase Polymerase Chain Reaction

RIPRNA immunoprecipitation

Electronic supplementary materialThe online version of this article doi:10.1186-s12943-017-0581-3 contains supplementary material, which is available to authorized users.

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Autor: Qin-nan Chen - Xin Chen - Zhen-yao Chen - Feng-qi Nie - Chen-chen Wei - Hong-wei Ma - Li Wan - Shuai Yan - Sheng-nan Ren

Fuente: https://link.springer.com/







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