Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE42945
PROVIDER: PRJNA184665 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR639445.fastq.gz | Fastqsanger.gz | |||
| SRR639446.fastq.gz | Fastqsanger.gz | |||
| SRR639447.fastq.gz | Fastqsanger.gz | |||
| SRR639448.fastq.gz | Fastqsanger.gz |
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Project description:Epstein-Barr virus (EBV) is a ubiquitous human herpesvirus associated with nasopharyngeal carcinoma (NPC). EBV encodes two groups of microRNAs (miRNAs) which are divided into BamHI fragment H rightward open reading frame 1 (BHRF1) and BamHI-A rightward transcripts (BART) microRNAs. EBV miR-BARTs have been found to be involved in the development and progression of NPC. However, the role of EBV-miR-BARTs in NPC progression remains illusive. This study aimed to investigate the role of EBV-miR-BARTs in NPC and explore the underlying mechanisms.
2019-11-27 | GSE118720 | GEO
Project description:Epstein-Barr virus (EBV) has been etiologically linked to human malignancies including Nasopharyngeal Carcinoma (NPC). Although EBV-encoded miRNAs have been shown to contribute to viral latency, host cell survival and immune evasion, their direct impact on cancer progression in their human host remains unclear. In the current study, based on a miRNA expression profiling analysis of a larger number of clinical specimens using a miRNA array platform containing human, EBV and other species miRNA probes., we found that some EBV-miR-BARTs were highly expressed in NPC. Accordingly, further exploration of the potential roles and regulatory mechanisms of some important EBV-miR-BARTs in NPC progression was carried out. We applied a miRNA expression profiling analysis in 20 poor or undifferentiated NPC (Nasopharyngeal Carcinoma) matched with 20 benign chronic nasopharyngitis (CNP) specimens using a miRNA array platform containing human, EBV and other species miRNA probes. Two-group experiment, NPC vs CNP. Biological repelicates: 20 NPCs, 20 CNPs. One replicate per array.
2015-06-30 | E-GEOD-43039 | biostudies-arrayexpress
Project description:Epstein-Barr virus (EBV) has been etiologically linked to human malignancies including Nasopharyngeal Carcinoma (NPC). Although EBV-encoded miRNAs have been shown to contribute to viral latency, host cell survival and immune evasion, their direct impact on cancer progression in their human host remains unclear. In the current study, based on a miRNA expression profiling analysis of a larger number of clinical specimens using a miRNA array platform containing human, EBV and other species miRNA probes., we found that some EBV-miR-BARTs were highly expressed in NPC. Accordingly, further exploration of the potential roles and regulatory mechanisms of some important EBV-miR-BARTs in NPC progression was carried out. We applied a miRNA expression profiling analysis in 20 poor or undifferentiated NPC (Nasopharyngeal Carcinoma) matched with 20 benign chronic nasopharyngitis (CNP) specimens using a miRNA array platform containing human, EBV and other species miRNA probes.
2015-06-30 | GSE43039 | GEO
Project description:<p>Nasopharyngeal carcinoma (NPC) is an aggressive head and neck cancer characterized by Epstein-Barr virus (EBV) infection and dense lymphocyte infiltration. The scarcity of NPC genomic data hinders the understanding of NPC biology, disease progression, and rational therapy design. Here, we performed whole-exome sequencing (WES) on 111 micro-dissected EBV-positive NPCs, with 15 cases subjected to further whole-genome sequencing (WGS), to determine its mutational landscape. We identified enrichment for genomic aberrations of multiple negative regulators of the NF-kB pathway in a total of 41% of cases including CYLD, TRAF3, NFKBIA and NLRC5. Functional analysis confirmed novel inactivating CYLD mutations as drivers for NPC cell growth. The EBV oncoprotein latent member protein 1 (LMP1) functions to constitutively activate NF-kB signaling, and we observed mutual exclusivity among somatic NF-kB pathway aberrations and LMP1-overexpression, suggesting that NF-kB activation is selected for by both somatic and viral events during NPC pathogenesis.</p>
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Project description:Nasopharyngeal carcinoma (NPC) is endemic in Southeast Asia and southern China. The primary treatment for NPC is radiotherapy. Despite of the encouraging results of radiotherapy, local recurrence or distant metastases of NPC after the initial therapy is frequently found due to radioresistance. Therefore, there is an urgent need to identify genes that control radiosensitivty, aiming to reduce disease recurrence. Epstein-Barr virus (EBV) infection was closely associated with undifferentiated NPC. EBV-encoded microRNAs (miRNAs) played crucial roles in the pathogenesis of NPC. Ebv-miR-BART7 belongs to the 44 EBV BART miRNAs and was found to be up-regulated in NPC tissues and plasma. Forced expression of ebv-miR-BART7 enhanced the radiosensitivity of NPC cells. However, the mechanisms underlying the sensitizing effect of ebv-miR-BART7 on radiation remain largely unknown. Given that miRNA exerts biological functions by regulating its targets, we used microarray to identify the targets of ebv-miR-BART7 that regulate radiosensitivity of NPC cells.
2017-03-31 | GSE79571 | GEO
Project description:Comprehensive Profiling of Epstein-Barr Virus-Encoded miRNAome Associated with Specific Latent Type in Tumor Cells Epstein-Barr virus (EBV) is an etiological cause of many human lymphocytic and epithelial malignancies. EBV expressed different genes associated with three latent types. So far as many as 44 EBV-encoded miRNA species have been found but their comprehensive and comparative profiling is not well documented in three latent infection states linked to various tumor cells. In this study, we utilized the polyA-tailed quantitative real time RT-PCR procedure to measure the relative abundance of viral miRNA species that linked to individual viral genome locations in combination with microarray evaluation in a subset of representative lymphoid and epithelial tumor cells undergoing various types of EBV latent infection. The results showed that miR-BHRF1 family and miR-BART family are expressed differentially in a tissue-dependent and latency-dependent manner. In particular, in NPC tissue and the only EBV consistently harboring cell line C666-1 with latency type II, there were highly abundant miR-BART family but not miR-BHRF1 family members that accounted for more than 10% of the whole known human miRNA library, implicating their important roles in maintaining EBV latent infection and driving NPC tumorigenesis. In addition, EBV miRNAome-based clustering analysis could classify three distinct EBV latency types, meanwhile, for the first time, we found and subsequently evaluated a novel secret latent switch in BL cell line Daudi from type I to III, which was unable to be identified by traditional latent biomarkers. Together, our data provided an in-depth and comparative profiling of EBV miRNA transcriptome in correspondence with three EBV latent infections, suggesting that different viral miRNA species were involved in divergent host cell carcinogenesis. Finally, EBV miRNAome, as a cluster of novel latency biomarkers expressed variedly in tumor cells, greatly complements and improves the classical typing criteria in conjunction with other latently expressed marker genes. 2 NPC tissue samples and 2 NPC cell lines and 5 lymphocytic cell lines
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Project description:MicroRNAs (miRNAs) represent a conserved class of small non-coding RNAs that are found in all higher eukaryotes as well as some DNA viruses. MiRNAs are 20-25 nucleotides (nt) in length and have important regulatory functions in biological processes such as embryonic development, cell differentiation, hormone secretion or metabolism. Furthermore, miRNAs have been implicated in the pathology of various diseases including cancer. MiRNA expression profiles not only classify different types of cancer but also may even help to characterize distinct tumor stages, therefore constituting a valuable tool for prognosis. Here we report the miRNA profile of Epstein-Barr Virus (EBV)-positive nasopharyngeal carcinoma (NPC) tissue samples characterized by cloning and sequencing. We find that all EBV miRNAs from the BART region are expressed in NPC tissues whereas ebv-miRNAs from the BHRF1 region are not found. Moreover, we identify two novel EBV miRNA genes originating from the BART region that have not been found in other tissues or cell lines before. We also identify three new human miRNAs, which might be specific for nasopharyngeal tissues. We further show that a number of different cellular miRNAs are upor down-regulated in NPC tissues compared to control tissue including miR-15a and miR-16. We find that the tumor suppressor BRCA-1 is a target of miR-15a as well as miR-16 suggesting a miRNA role in NPC pathogenesis. 2 pairs of NPC and control tissues from 2 patients (4 samples in total) were examined.
2009-02-07 | E-GEOD-14738 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) represent a conserved class of small non-coding RNAs that are found in all higher eukaryotes as well as some DNA viruses. MiRNAs are 20-25 nucleotides (nt) in length and have important regulatory functions in biological processes such as embryonic development, cell differentiation, hormone secretion or metabolism. Furthermore, miRNAs have been implicated in the pathology of various diseases including cancer. MiRNA expression profiles not only classify different types of cancer but also may even help to characterize distinct tumor stages, therefore constituting a valuable tool for prognosis. Here we report the miRNA profile of Epstein-Barr Virus (EBV)-positive nasopharyngeal carcinoma (NPC) tissue samples characterized by cloning and sequencing. We find that all EBV miRNAs from the BART region are expressed in NPC tissues whereas ebv-miRNAs from the BHRF1 region are not found. Moreover, we identify two novel EBV miRNA genes originating from the BART region that have not been found in other tissues or cell lines before. We also identify three new human miRNAs, which might be specific for nasopharyngeal tissues. We further show that a number of different cellular miRNAs are upor down-regulated in NPC tissues compared to control tissue including miR-15a and miR-16. We find that the tumor suppressor BRCA-1 is a target of miR-15a as well as miR-16 suggesting a miRNA role in NPC pathogenesis.
2009-02-07 | GSE14738 | GEO
Project description:Unlike other EBV-associated human tumors, nearly 100% wild-type p53 gene is found in NPC, p53 protein is also frequently found to accumulate in NPC biopsies. However, the role of p53 in EBV-positive nasopharyngeal carcinoma is unclear. The expression profiles of mRNAs and miRNAs of EBV-positive NPC cells are unknown. To elucidate the function of p53 in EBV-positive NPC, we used the CRISPR-Cas9 gene editing system to p53 knockout C666-1 cells with Epstein-Barr virus and performed mRNA and miRNA sequencing in p53 KO C666-1 and their control cells. Gene Ontology (GO), KEGG and STRING analyses were implemented to identify significant functions, pathways of differentially expressed mRNAs. Through comparative analysis of p53-regulated genes from EBV-positive C666-1 cells and EBV-negative HONE2 cells with p53 target genes from 16 high throughput data sets, we found that the number of target genes and KEGG pathways downregulated by p53 in EBV-positive C666-1 cells were much less than in EBV-negative HONE2 cells, but “p53 signaling pathway” and related cell cycle arrest and apoptosis genes were significantly downregulated after knockout of p53 gene in C666-1 cells. To explore the effect of p53 on cell cycle and apoptosis, we established stable p53 C666-1-KO cell lines with stable expression of exogenous p53-WT and their control cell lines. Using the established cell lines, we observed that stable expression of p53 repressed cell proliferation, increased cell apoptosis and blocked G1/S phase progression. In conclusion, our results show that the accumulated p53 protein in EBV-positive C666-1 cells still has some tumour suppressor functions such as blocking cell-cycle progression and promoting apoptosis, but the ability of p53 to downregulate gene expression is inhibited.
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