Abstract
BackgroundNon-small cell lung cancer (NSCLC) is one of the leading causes of cancer death in the world, and has a relatively low survival rate. Long non-coding RNAs (lncRNAs) have been demonstrated to modulate cancer progression through a variety of molecular mechanisms. We sought to investigate the role and potential mechanism of MYC-induced long non-coding RNA (MINCR) in NSCLC.MethodsExpression levels of MINCR was first identified using The Cancer Genome Atlas (TCGA), further confirmed with specimens from 29 NSCLC patients and three cell lines using qRT-PCR. Overexpression and knockdown of MINCR were performed in NSCLC cell lines through MINCR overexpression vectors and synthesized siRNAs, respectively. The roles of MINCR in NSCLC cell lines, such as cell proliferation, cell cycle arrest, and apoptosis, were identified by MTT, flow cytometry, and Western blot. The modulation of MINCR-regulated genes, including c-Myc and its downstream effectors, as well as apoptosis-associated genes, was analyzed using Western blot.ResultsMINCR expression was increased in NSCLC patients from TCGA datasets, and was also significantly increased in our collected specimens from NSCLC patients and NSCLC cell lines. Knocking down of MINCR greatly inhibited the growth of NSCLC cell lines PC9 and A549. In addition, silencing of MINCR induced cell cycle arrest and apoptosis. Furthermore, silencing of MINCR reduced the expression levels of oncogene c-Myc and its downstream cyclin A, cyclin D, CD4, and CDK2, as well as apoptosis-associated Bcl-2, while significantly increased the expression levels of cleaved PARP-1. In the meantime, overexpression of MINCR remarkably enhanced cell proliferation of PC9 cells and activated c-Myc and its downstream effectors.ConclusionMINCR exerted inhibitory effects on the cell cycle arrest and apoptosis of NSCLC cells by activating c-Myc and its downstream effectors, suggesting that this lncRNA could be used as a potential therapeutic target for the treatment of NSCLC.
Highlights
Lung cancer is one of the leading causes of malignancy induced human death
We evaluated the function of MYC-induced long non-coding RNA (MINCR) in the proliferation and apoptosis of Non-small cell lung cancer (NSCLC) cell lines in vitro, and investigated the impact of MINCR on oncogene c-Myc and its downstream effectors, as well as apoptosis-associated genes to reveal the underlying mechanism beneath these phenomena
MINCR expression was increased in NSCLC tissues and cell lines The expression of MINCR in clinical lung cancers, including lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC), was first identified using The Cancer Genome Atlas (TCGA) dataset
Summary
Lung cancer is one of the leading causes of malignancy induced human death. Chen et al Respiratory Research (2019) 20:202 without protein-coding potential [2,3,4]. It has been revealed that lncRNAs are very heterogeneous in their mechanisms of function. Without any surprise, as the researches go on, lncRNAs have been demonstrated to exhibit versatile functions in diverse biological processes [5,6,7,8]. Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer death in the world, and has a relatively low survival rate. Long non-coding RNAs (lncRNAs) have been demonstrated to modulate cancer progression through a variety of molecular mechanisms. We sought to investigate the role and potential mechanism of MYC-induced long non-coding RNA (MINCR) in NSCLC
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