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Long non-coding RNA dysregulation is a frequent event in non-small cell lung carcinoma pathogenesis

ABSTRACT: Long non-coding RNA dysregulation is a frequent event in non-small cell lung carcinoma pathogenesis

PROVIDER: PRJNA541245 | ENA |

REPOSITORIES: ENA

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Long non-coding RNA dysregulation is a frequent event in non-small cell lung carcinoma pathogenesis.

Project description:BackgroundLong non-coding RNAs compose an important level of epigenetic regulation in normal physiology and disease. Despite the plethora of publications of lncRNAs in human cancer, the landscape is still unclear.MethodsMicroarray analysis in 44 NSCLC paired specimens was followed by qPCR-based validation in 29 (technical) and 38 (independent) tissue pairs. Cross-validation of the selected targets was achieved in 850 NSCLC tumours from TCGA datasets.ResultsTwelve targets were successfully validated by qPCR (upregulated: FEZF1-AS1, LINC01214, LINC00673, PCAT6, NUTM2A-AS1, LINC01929; downregulated: PCAT19, FENDRR, SVIL-AS1, LANCL1-AS1, ADAMTS9-AS2 and LINC00968). All of them were successfully cross validated in the TCGA datasets. Abnormal DNA methylation was observed in the promoters of FENDRR, FEZF1-AS1 and SVIL-AS1. FEZF1-AS1 and LINC01929 were associated with survival in the TCGA set.ConclusionsOur study provides through multiple levels of internal and external validation, a comprehensive list of dysregulated lncRNAs in NSCLC. We therefore envisage this dataset to serve as an important source for the lung cancer research community assisting future investigations on the involvement of lncRNAs in the pathogenesis of the disease and providing novel biomarkers for diagnosis, prognosis and therapeutic stratification.

| S-EPMC7109049 | biostudies-literature

Long non-coding RNA dysregulation is a frequent event in non-small cell lung carcinoma pathogenesis

Project description:Our aim was to contribute to a more comprehensive landscape for lncRNA deregulation in NSCLC by identifying lncRNA profiles that could significantly discriminate NSCLCs tissue from paired normal lung tissue. Therefore, we assessed the transcriptional profile of 44 paired tumour and adjacent normal lung tissue from NSCLC patients using an Agilent Custom 8x60K expression array (AMADID: 047718) designed by the GENCODE consortium. This microarray, based on the Gencode v15 catalog of human lncRNA, interrogates 17,535 randomly selected protein coding and 22,001 lncRNA transcripts, being each transcript targeted by two probes.

2019-12-09 | GSE130740 | GEO

Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma

Project description:Purpose: Nasopharyngeal carcinoma (NPC) is a common malignant carcinoma of the head and neck, and the biological mechanisms underlying the pathogenesis of NPC remain not fully understood.Thus, more studies are needed to identify novel critical molecular events and key hub genes to develop novel diagnostic and therapeutic strategies for the management and treatment of NPC. Methods: In the present study, we systematically analyzed four independent NPC transcriptomic da-tasets and focused on identifying the critical molecular networks and novel key hub genes implicated in NPC. We found totally 170 common overlapping differentially expressed genes (DEGs) in the four NPC datasets. GO and KEGG pathway analysis revealed that cell cycle dysregulation is a critical event in NPC. Protein-protein interaction (PPI) network analysis identified a 15 hub-gene core network with overexpressed kinesin family member 2C (KIF2C) as a central regulator. Results: Loss-of-function study demonstrated that knockdown of KIF2C significantly inhibited cell growth and cell motility, and delayed cell cycle progression, accompanied with dramatic mitotic defects in spindle formation in NPC cells. RNA-seq analysis revealed that KIF2C knockdown led to deregulation of various downstream genes. KIF2C could also regulate the AKT/mTOR pathways, and enhance paclitaxel sensitivity in NPC cells. Conclusions: Taken together, our results suggest that cell cycle dysregulation is a critical event during NPC pathogenesis and KIF2C is a novel key mitotic hub gene with therapeutic potential in NPC.

2021-06-10 | GSE176471 | GEO

RNA splicing dysregulation in the pathogenesis of chronic lymphocytic leukemia

Project description:RNA splicing dysregulation in the pathogenesis of chronic lymphocytic leukemia

| PRJNA930121 | ENA

RNA splicing dysregulation in the pathogenesis of chronic lymphocytic leukemia

Project description:RNA splicing dysregulation in the pathogenesis of chronic lymphocytic leukemia

| PRJNA930122 | ENA

Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma

Project description:Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma

| PRJNA736377 | ENA

Dysregulation of PDGFRB contributes to the pathogenesis of LMNA-related dilated cardiomyopathy

Project description:Dysregulation of PDGFRB contributes to the pathogenesis of LMNA-related dilated cardiomyopathy

| PRJNA487115 | ENA

Transcriptome networks identify susceptibility to frequent asthma exacerbations

Project description:To investigate mechanisms underlying frequent asthma exacerbation, we profiled the nasal transcriptome of both frequent and non-frequent asthma exacerbators.

2023-10-17 | GSE211158 | GEO

Chromothripsis is a frequent event and underlies typical genetic changes in early T-cell precursor lymphoblastic leukemia in adults

Project description:Chromothripsis is a frequent event and underlies typical genetic changes in early T-cell precursor lymphoblastic leukemia in adults

| PRJNA844306 | ENA

Dysregulation of RBFOX2 Is an Early Event in Cardiac Pathogenesis of Diabetes.

Project description:Alternative splicing (AS) defects that adversely affect gene expression and function have been identified in diabetic hearts; however, the mechanisms responsible are largely unknown. Here, we show that the RNA-binding protein RBFOX2 contributes to transcriptome changes under diabetic conditions. RBFOX2 controls AS of genes with important roles in heart function relevant to diabetic cardiomyopathy. RBFOX2 protein levels are elevated in diabetic hearts despite low RBFOX2 AS activity. A dominant-negative (DN) isoform of RBFOX2 that blocks RBFOX2-mediated AS is generated in diabetic hearts. DN RBFOX2 interacts with wild-type (WT) RBFOX2, and ectopic expression of DN RBFOX2 inhibits AS of RBFOX2 targets. Notably, DN RBFOX2 expression is specific to diabetes and occurs at early stages before cardiomyopathy symptoms appear. Importantly, DN RBFOX2 expression impairs intracellular calcium release in cardiomyocytes. Our results demonstrate that RBFOX2 dysregulation by DN RBFOX2 is an early pathogenic event in diabetic hearts.

| S-EPMC4899142 | biostudies-other

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