scholarly journals Identification of Potential Long Non-coding RNA Expression Quantitative Trait Methylations in Lung Adenocarcinoma and Lung Squamous Carcinoma

2020 ◽  
Vol 11 ◽  
Author(s):  
Xiaohong Wu ◽  
Yue Gao ◽  
Jianlong Bu ◽  
Lin Deng ◽  
Pinyi Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Quantitative Trait ◽  
Regulatory Networks ◽  
Squamous Carcinoma ◽  
Drug Repurposing ◽  
Cancer Pathogenesis ◽  
Non Coding Rna ◽  
Wide Range ◽  
Lung Squamous Carcinoma ◽  
Long Non Coding Rna

There are associations between DNA methylation and the expression of long non-coding RNA (lncRNA), also known as lncRNA expression quantitative trait methylations (lnc-eQTMs). Lnc-eQTMs may induce a wide range of carcinogenesis pathways. However, lnc-eQTMs have not been globally identified and studied, and their roles in lung adenocarcinoma (LUAD) and lung squamous carcinoma (LUSC) are largely unknown. In the present study, we identified some differential methylation sites located in genes of long intergenic non-coding RNAs (lincRNAs) and other types of lncRNAs in LUAD and LUSC. An integrated pipeline was established to construct two global cancer-specific regulatory networks of lnc-eQTMs in LUAD and LUSC. The associations between eQTMs showed common and specific features between LUAD and LUSC. Some lnc-eQTMs were also related with survival in LUAD- and LUSC-specific regulatory networks. Lnc-eQTMs were associated with cancer-related functions, such as lung epithelium development and vasculogenesis by functional analysis. Drug repurposing analysis revealed that these lnc-eQTMs may mediate the effects of some anesthesia-related drugs in LUAD and LUSC. In summary, the present study elucidates the roles of lnc-eQTMs in LUAD and LUSC, which could improve our understanding of lung cancer pathogenesis and facilitate treatment.

scholarly journals PD-L1 lncRNA splice isoform promotes lung adenocarcinoma progression via enhancing c-Myc activity

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuang Qu ◽  
Zichen Jiao ◽  
Geng Lu ◽  
Bing Yao ◽  
Ting Wang ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Lung Adenocarcinoma ◽  
Solid Tumors ◽  
Immune Checkpoint ◽  
Checkpoint Inhibition ◽  
Immune Checkpoint Inhibition ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Lung Adenocarcinoma Cells ◽  
Long Non Coding Rna

Abstract Background Although using a blockade of programmed death-ligand 1 (PD-L1) to enhance T cell immune responses shows great promise in tumor immunotherapy, the immune-checkpoint inhibition strategy is limited for patients with solid tumors. The mechanism and efficacy of such immune-checkpoint inhibition strategies in solid tumors remains unclear. Results Employing qRT-PCR, Sanger sequencing, and RNA BaseScope analysis, we show that human lung adenocarcinoma (LUAD) all produce a long non-coding RNA isoform of PD-L1 (PD-L1-lnc) by alternative splicing, regardless if the tumor is positive or negative for the protein PD-L1. Similar to PD-L1 mRNA, PD-L1-lnc in various lung adenocarcinoma cells is significantly upregulated by IFNγ. Both in vitro and in vivo studies demonstrate that PD-L1-lnc increases proliferation and invasion but decreases apoptosis of lung adenocarcinoma cells. Mechanistically, PD-L1-lnc promotes lung adenocarcinoma progression through directly binding to c-Myc and enhancing c-Myc transcriptional activity. Conclusions In summary, the PD-L1 gene can generate a long non-coding RNA through alternative splicing to promote lung adenocarcinoma progression by enhancing c-Myc activity. Our results argue in favor of investigating PD-L1-lnc depletion in combination with PD-L1 blockade in lung cancer therapy.

scholarly journals LncRNA-MALAT1-mediated Axl promotes cell invasion and migration in human neuroblastoma

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831769979 ◽  
Author(s):  
Shaojie Bi ◽  
Chunyan Wang ◽  
Yixin Li ◽  
Wei Zhang ◽  
Juan Zhang ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Invasion ◽  
Neuroblastoma Cells ◽  
Great Influence ◽  
Regulatory Mechanisms ◽  
Human Neuroblastoma ◽  
Invasion And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna

Overexpression of Axl has been noted to correlate with several human cancers. However, the regulatory mechanisms and effects of Axl in human neuroblastoma development remain unclear. Here, we explore the expression of Axl in neurobalstoma and related upstream regulatory mechanisms of invasion and migration. We found that Axl was overexpressed in metastatic neuroblastoma tissues and positively associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1. Meanwhile, our data suggested that metastasis-associated lung adenocarcinoma transcript 1 upregulated Axl expression in neuroblastoma cells, resulting in cell invasion and migration. Furthermore, we found that targeting Axl by inhibitor R428 significantly suppressed the abilities of tumor cell invasion and migration. In summary, these results suggested that Axl, which is regulated by long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1, may exert great influence on invasion and migration of neuroblastoma.

scholarly journals Down-regulated LncR-MALAT1 suppressed cell proliferation and migration by inactivating autophagy in bladder cancer

RSC Advances ◽  
2018 ◽  
Vol 8 (54) ◽  
pp. 31019-31027
Author(s):  
Jiude Qi ◽  
Yanfeng Chu ◽  
Guangyan Zhang ◽  
Hongjun Li ◽  
Dongdong Yang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Bladder Cancer ◽  
Lung Adenocarcinoma ◽  
Tumor Cells ◽  
Cell Proliferation And Migration ◽  
Non Coding Rna ◽  
And Migration ◽  
Long Non Coding Rna ◽  
Proliferation And Migration

Long non-coding RNA-metastasis-associated lung adenocarcinoma transcript (LncR-MALAT) is highly expressed in a variety of tumors, which can affect the progression of tumor cells.

scholarly journals Positional cloning of quantitative trait nucleotides for blood pressure and cardiac QT-interval by targeted CRISPR/Cas9 editing of a novel long non-coding RNA

PLoS Genetics ◽  
2017 ◽  
Vol 13 (8) ◽  
pp. e1006961 ◽  
Author(s):  
Xi Cheng ◽  
Harshal Waghulde ◽  
Blair Mell ◽  
Eric E. Morgan ◽  
Shondra M. Pruett-Miller ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Quantitative Trait ◽  
Qt Interval ◽  
Positional Cloning ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract 051: A Panel of CRISPR/Cas9 Genome Edited Rat Models Define Quantitative Trait Nucleotides within a Novel Rat Long Non-coding RNA Implicated in Cardiovascular Disease

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Xi Cheng ◽  
Harshal Waghulde ◽  
Blair Mell ◽  
Shondra Miller ◽  
Wanda Filipiak ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Quantitative Trait ◽  
Qt Interval ◽  
Chromosome 17 ◽  
Insertion Polymorphism ◽  
Non Coding Rna ◽  
Trait Locus ◽  
Human Chromosome 17 ◽  
Long Non Coding Rna

This study is focused on a GWAS locus for cardiovascular disease (QT-interval) on human chromosome 17. The homologous genomic segment of this human locus was previously mapped with high resolution to <42.5 kb on rat chromosome 10. The locus in rats regulates both QT-interval and blood pressure and contains a novel long non-coding RNA (lncRNA), with a large 19bp deletion/insertion polymorphism observed between the strains used to map the locus. Characterization of this novel lncRNA using rapid amplification of cDNA ends (RACE) provided evidence for the presence of more than a single isoform of the lncRNA. To further assess the role of this locus, a panel of CRISPR/Cas9 based gene-edited ‘knockout’ models of the lncRNA was developed. The lncRNA targeted rats were developed on the genomic background of the hypertensive Dahl salt-sensitive rats and harbored varied disruptions around the critical 19bp region. The rat strains with the disrupted lncRNA sequences had a significantly elevated blood pressure compared with the controls. QT-interval is currently being examined. Overall, this is the first demonstration of a CRISPR/Cas9 based targeted gene-editing approach applied to identify a novel lncRNA as a Blood Pressure Quantitative Trait Locus.

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