scholarly journals Long non-coding RNA LINC00987 may function as a tumor suppressor in lung adenocarcinoma

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 540
Author(s):  
Abbas Salavaty ◽  
Zahra Rezvani ◽  
Ali Najafi
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cancer Type ◽  
Online Databases ◽  
Non Coding Rna ◽  
Genome Consortium ◽  
Data Portal ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Bioinformatic Approach

Long non-coding RNAs (lncRNAs) are a group of transcripts over 200 nucleotides in length that do not code for proteins. The association of the dysregulation of numerous lncRNAs with several malignancies, including lung cancer, has been frequently reported. This study aims to inspect the association of genomic and transcriptomic alterations to the lncRNA LINC00987 with lung adenocarcinoma, a subtype of lung cancer, using a bioinformatic approach. To this end, we used three publically available online databases, cBioPortal, the International Cancer Genome Consortium Data Portal and the GEPIA web server. In short, our results demonstrated that LINC00987 expression might have a tumor suppressive role in lung adenocarcinoma and levels of expression could be of prognostic value for this cancer type.

scholarly journals Long non-coding RNA LINC01559 exerts oncogenic role via enhancing autophagy in lung adenocarcinoma

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhuochen Zhao ◽  
Junhu Wan ◽  
Manman Guo ◽  
Zhengwu Yang ◽  
Zhuofang Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cancer Cell Proliferation ◽  
Lasso Regression ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Selection Operator ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNAs (lncRNAs) have been verified to play fatal role in regulating the progression of lung adenocarcinoma (LUAD). Although lncRNAs play important role in regulating the autophagy of tumor cells, the function and molecular mechanism of LINC01559 in regulating lung cancer development remain to be elucidated. Method and materials In this study, we used bioinformatics to screen out autophagy-related lncRNAs from TCGA-LUAD repository. Then the least absolute shrinkage and selection operator (LASSO) regression was applied to establish the signature of autophagy-related lncRNAs so that clinical characteristics and survival in LUAD patients be evaluated. Finally, we selected the most significant differences lncRNA, LINC01559, to verify its function in regulating LUAD progression in vitro. Results We found high expression of LINC01559 indicates lymph node metastasis and poor prognosis. Besides, LINC01559 promotes lung cancer cell proliferation and migration in vitro, by enhancing autophagy signal pathway via sponging hsa-miR-1343-3p. Conclusion We revealed a novel prognostic model based on autophagy-related lncRNAs, and provide a new therapeutic target and for patients with lung adenocarcinoma named LINC01559.

scholarly journals Long Non-Coding RNA LINC01559 Exerts Oncogenic Role Via Enhancing Autophagy in Lung Adenocarcinoma

2021 ◽  
Author(s):  
Zhuochen Zhao ◽  
Junhu Wan ◽  
Manman Guo ◽  
Zhengwu Yang ◽  
Zhuofang Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Cancer Cell Proliferation ◽  
Lasso Regression ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Selection Operator ◽  
Long Non Coding Rna

Abstract Background: Long non-coding RNAs (lncRNAs) have been verified to play fatal role in regulating the progression of lung adenocarcinoma (LUAD). Although lncRNAs play important role in regulating the autophagy of tumor cells, the function and molecular mechanism of LINC01559 in regulating lung cancer development remain to be elucidated. Method and materials: In this study, we used bioinformatics to screen out autophagy-related lncRNAs from TCGA-LUAD repository, and the least absolute shrinkage and selection operator (LASSO) regression was applied to establish the clinical characteristics and survival of autophagy-related lncRNAs in LUAD patients was analyzed. Finally, we selected the most significant differences lncRNA, LINC01559, to verify its function in regulating LUAD progression.Results: we found high expression of LINC01559 indicates lymph node metastasis and poor prognosis. Besides, LINC01559 promotes lung cancer cell proliferation and migration in vitro, by enhancing autophagy signal pathway. Conclusion: We revealed a novel prognostic model based on autophagy-related lncRNAs, and provide a new therapeutic target and for patients with lung adenocarcinoma with LINC01559.

scholarly journals Autophagy‐related Long Non-coding RNA Signature Associated with Prognosis of Lung Adenocarcinoma

2021 ◽  
Author(s):  
Guofei Zhang ◽  
Jiayi Shen ◽  
Zipu Yu ◽  
Gang Shen ◽  
Chengxiao Liang
Keyword(s):  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Cox Regression ◽  
Microarray Dataset ◽  
Risk Groups ◽  
The Cancer Genome Atlas ◽  
Non Coding Rna ◽  
Cancer Genome Atlas ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Abstract BackgroundEvidence suggests that long non-coding RNAs (lncRNAs) are involved in various cancers. Here, we developed and evaluated an autophagy-related prognostic lncRNA signature for lung adenocarcinoma (LUAD). ResultsUsing a publicly available microarray dataset from The Cancer Genome Atlas, we analyzed the lncRNA expression profile in a cohort of 439 LUAD patients. The lncRNA-mRNA co-expression network along with univariate and multivariate Cox regression analyses were used to determine 15 autophagy-related lncRNA signatures that were significantly correlated with patient overall survival. Autophagy-related lncRNA signatures stratified patients into high- and low-risk groups with significantly different survival (hazard ratio = 3.256, 95% confidence interval = 2.858–4.101, P < 0.001). The lncRNA signature was further confirmed in other independent datasets. Moreover, the lncRNA signature had prognostic value independent of routine clinical factors. Functional analysis indicated that autophagy-related lncRNA signatures may be involved in LUAD via known autophagy-related pathways. ConclusionsThis newly identified autophagy-related lncRNA signature is a more powerful prognostic tool than the clinicopathological factors routinely used to predict patient survival, and can provide further insights into the molecular mechanisms underlying LUAD.

CCAT2 is a lung adenocarcinoma-specific long non-coding RNA and promotes invasion of non-small cell lung cancer

Tumor Biology ◽  
2014 ◽  
Vol 35 (6) ◽  
pp. 5375-5380 ◽  
Author(s):  
Mantang Qiu ◽  
Youtao Xu ◽  
Xin Yang ◽  
Jie Wang ◽  
Jingwen Hu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Lung Adenocarcinoma ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Non Coding Rna ◽  
Long Non Coding Rna

scholarly journals Long non-coding RNA LINC00485 acts as a microRNA-195 sponge to regulate the chemotherapy sensitivity of lung adenocarcinoma cells to cisplatin by regulating CHEK1

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Zuo ◽  
Wei Zhang ◽  
Fei Xu ◽  
Jing Zhou ◽  
Wei Bai
Keyword(s):  
Lung Adenocarcinoma ◽  
Protein Coding ◽  
Chemotherapy Sensitivity ◽  
Over Expression ◽  
Non Coding Rna ◽  
Adenocarcinoma Cells ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Competitive Endogenous Rna

Abstract Background Long non-coding RNAs (lncRNAs) are a family of non-protein-coding RNAs, which have the ability to influence the chemo-resistance of lung adenocarcinoma (LAC). In this study, we explored the mechanism by which LINC00485 competitively binds to microRNA-195 (miR-195) in the regulation of the chemotherapy sensitivity in LAC by regulating checkpoint kinase 1 (CHEK1). Methods Microarray analysis was used to screen out LAC related genes, and interaction between CHEK1 and miR-195, as well as that between miR-195 and LINC00485, was further confirmed by RNA-pull down and RIP. LINC00485 expression in LAC cells (A549 and H1299) was determined. The cells were then introduced with miR-195, anta-miR-195, LINC00485 or si-LINC00485 to identify the role of miR-195 and LINC00485 in LAC through evaluating the expression of CHEK1, CHEK1, Bax, Bcl-2, VEGF and HIF-1α in LAC cells by either RT-qPCR or Western blot analysis. After being treated with different concentration of cisplatin, cell proliferation, colony formation and apoptosis were assessed. Results LINC00485 acted as a competitive endogenous RNA against miR-195, and miR-195 directly targeted CHEK1. The expression of LINC00485 was higher in LAC cells. The down-regulation of LINC00485 or the up-regulation of miR-195 decreased the expression of CHEK1, Bcl-2, VEGF and HIF-1α, while also increasing the expression of Bax. Moreover, the over-expression of miR-195, or the silencing of LINC00485 enhanced the sensitivity of LAC cells to cisplatin, thereby promoting the apoptosis of LAC cells while suppressing the proliferation. Conclusion LINC00485 competitively binds to miR-195 to elevate CHEK1 expression in LAC cells, suggesting that LINC00485 is a novel direction for therapeutic strategies of LAC.

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 Long Non-coding RNA FEZF1-AS1 Promotes Growth and Reduces Apoptosis Through Regulation of miR-363-3p/PAX6 Axis in Retinoblastoma

2021 ◽  
Author(s):  
Xiuming Liu ◽  
Xiaofeng Li ◽  
Jianchang Li
Keyword(s):  
Cell Viability ◽  
Antisense Rna ◽  
Tumor Formation ◽  
Retinoblastoma Cell ◽  
Non Coding Rna ◽  
High Incidence ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Common Malignancy

AbstractRetinoblastoma is the most common malignancy in children's eyes with high incidence. Long non-coding RNAs (lncRNAs) play important roles in the progression of retinoblastoma. LncRNA FEZF1 antisense RNA 1 (FEZF1-AS1) has been found to stimulate retinoblastoma. However, the mechanism of FEZF1-AS1 underlying progression of retinoblastoma is still unclear. In current study, FEZF1-AS1 was up-regulated in retinoblastoma tissues and cells. FEZF1-AS1 overexpression enhanced retinoblastoma cell viability, promoted cell cycle, and inhibited apoptosis. Conversely, FEZF1-AS1 knockdown reduced cell viability, cycle, and elevated apoptosis. The interaction between FEZF1-AS1 and microRNA-363-3p (miR-363-3p) was confirmed. FEZF1-AS1 down-regulated miR-363-3p and up-regulated PAX6. PAX6 was a target gene of miR-363-3p. EZF1-AS1 promoted retinoblastoma cell viability and suppressed apoptosis via PAX6. Further, we demonstrated that FEZF1-AS1 contribute to tumor formation in vivo. In conclusion, FEZF1-AS1 elevated growth and inhibited apoptosis by regulating miR-363-3p/PAX6 in retinoblastoma, which provide a new target for retinoblastoma treatment.

scholarly journals Long non-coding RNA AFAP1-AS1 accelerates lung cancer cells migration and invasion by interacting with SNIP1 to upregulate c-Myc

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Yu Zhong ◽  
Liting Yang ◽  
Fang Xiong ◽  
Yi He ◽  
Yanyan Tang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Cancer Metastasis ◽  
Lung Cancer Cells ◽  
Migration And Invasion ◽  
Lung Cancer Patients ◽  
Lung Cancer Metastasis ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractActin filament associated protein 1 antisense RNA 1 (named AFAP1-AS1) is a long non-coding RNA and overexpressed in many cancers. This study aimed to identify the role and mechanism of AFAP1-AS1 in lung cancer. The AFAP1-AS1 expression was firstly assessed in 187 paraffin-embedded lung cancer and 36 normal lung epithelial tissues by in situ hybridization. The migration and invasion abilities of AFAP1-AS1 were investigated in lung cancer cells. To uncover the molecular mechanism about AFAP1-AS1 function in lung cancer, we screened proteins that interact with AFAP1-AS1 by RNA pull down and the mass spectrometry analyses. AFAP1-AS1 was highly expressed in lung cancer clinical tissues and its expression was positively correlated with lung cancer patients’ poor prognosis. In vivo experiments confirmed that AFAP1-AS1 could promote lung cancer metastasis. AFAP1-AS1 promoted lung cancer cells migration and invasion through interacting with Smad nuclear interacting protein 1 (named SNIP1), which inhibited ubiquitination and degradation of c-Myc protein. Upregulation of c-Myc molecule in turn promoted the expression of ZEB1, ZEB2, and SNAIL gene, which ultimately enhanced epithelial to mesenchymal transition (EMT) and lung cancer metastasis. Understanding the molecular mechanism by which AFAP1-AS1 promotes lung cancer’s migration and invasion may provide novel therapeutic targets for lung cancer patients’ early diagnosis and therapy.

scholarly journals Integrated Analysis of Long Non-Coding RNA and mRNA Expression Profiles in Testes of Calves and Sexually Mature Wandong Bulls (Bos taurus)

Animals ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 2006
Author(s):  
Hongyu Liu ◽  
Ibrar Muhammad Khan ◽  
Huiqun Yin ◽  
Xinqi Zhou ◽  
Muhammad Rizwan ◽  
...  
Keyword(s):  
Target Genes ◽  
Expression Profiles ◽  
Age Groups ◽  
Adherens Junction ◽  
Integrated Analysis ◽  
Sequencing Data ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Rna Interaction ◽  
Long Non Coding Rna

The mRNAs and long non-coding RNAs axes are playing a vital role in the regulating of post-transcriptional gene expression. Thereby, elucidating the expression pattern of mRNAs and long non-coding RNAs underlying testis development is crucial. In this study, mRNA and long non-coding RNAs expression profiles were investigated in 3-month-old calves and 3-year-old mature bulls’ testes by total RNA sequencing. Additionally, during the gene level analysis, 21,250 mRNAs and 20,533 long non-coding RNAs were identified. As a result, 7908 long non-coding RNAs (p-adjust < 0.05) and 5122 mRNAs (p-adjust < 0.05) were significantly differentially expressed between the distinct age groups. In addition, gene ontology and biological pathway analyses revealed that the predicted target genes are enriched in the lysine degradation, cell cycle, propanoate metabolism, adherens junction and cell adhesion molecules pathways. Correspondingly, the RT-qPCR validation results showed a strong consistency with the sequencing data. The source genes for the mRNAs (CCDC83, DMRTC2, HSPA2, IQCG, PACRG, SPO11, EHHADH, SPP1, NSD2 and ACTN4) and the long non-coding RNAs (COX7A2, COX6B2, TRIM37, PRM2, INHBA, ERBB4, SDHA, ATP6VOA2, FGF9 and TCF21) were found to be actively associated with bull sexual maturity and spermatogenesis. This study provided a comprehensive catalog of long non-coding RNAs in the bovine testes and also offered useful resources for understanding the differences in sexual development caused by the changes in the mRNA and long non-coding RNA interaction expressions between the immature and mature stages.

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