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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.

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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.

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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.

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

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

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