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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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NPC stem-like cells [Affymetrix]

ABSTRACT: Stem-like cells of nasopharyngeal cancer were enriched by 3 different methods: 1) Side population (SP) assay, 2) LMP2A over-expression and 3) spheroid culture. SP cells and LMP2A over-expressed cells were inoculated into immunocompromised mice for xenograft tumors. Transcriptomes of all 5 of these in vitro and in vivo generated NPC stem-like cells were then analyzed and compared to their counterparts by microarray. All samples were analyzed in the Agilent platform except the SP cells and their counterpart (analyzed in the Affymetrix platform). Three RNA sample replicates were prepared from each type of the NPC stem-like cells and their counterpart.

ORGANISM(S): Homo sapiens

SUBMITTER: Lu Ping Tan

PROVIDER: E-GEOD-36125 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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NPC stem-like cells [Agilent]

Project description:Stem-like cells of nasopharyngeal cancer were enriched by 3 different methods: 1) Side population (SP) assay, 2) LMP2A over-expression and 3) spheroid culture. SP cells and LMP2A over-expressed cells were inoculated into immunocompromised mice for xenograft tumors. Transcriptomes of all 5 of these in vitro and in vivo generated NPC stem-like cells were then analyzed and compared to their counterparts by microarray. All samples were analyzed in the Agilent platform except the SP cells and their counterpart (analyzed in the Affymetrix platform).

2023-02-04 | GSE36124 | GEO

NPC stem-like cells [Affymetrix]

2023-02-04 | GSE36125 | GEO

Transcriptome sequencing of nasopharyngeal carcinoma model system (miRNA)

Project description:Nasopharyngeal carcinoma (NPC) is a prevalent malignancyt disease in Southeast Asia among the Chinese population. Aberrant regulation of transcripts has been implicated in many types of cancers including NPC. Herein, we characterized mRNA and miRNA transcriptomes by RNA sequencing (RNASeq) of NPC model systems. Matched total mRNA and small RNA of undifferentiated Epstein-Barr virus (EBV)-positive NPC xenograft X666 and its derived cell line C666, well-differentiated NPC cell line HK1, and the immortalized nasopharyngeal epithelial cell line NP460 have been sequenced by Solexa technology.

2014-02-05 | E-GEOD-54161 | biostudies-arrayexpress

Transcriptome sequencing of nasopharyngeal carcinoma model system (mRNA)

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Expression data from EBV-encoded latent membrane protein 2A (LMP2A) positive and negative nasopharyngeal carcinoma (NPC) cell lines

Project description:Latent infection with Epstein-Barr virus (EBV) is recognised as a factor in the pathogenesis of nasopharyngeal carcinoma (NPC). We found that EBV encoded Latent membrane protein 2A (LMP2A) enhances lipid accumulation significantly in NPC cells. We used microarrays to identify differential genes regulated by LMP2A in NPC cell lines.

2018-08-21 | GSE118807 | GEO

ABBERANT GENE EXPRESSION BY EBERs IN EBV-NEGATIVE NPC HK1 CELL LINE

Project description:Differential gene expression in RNA isolated from stably-transfected EBERs-negative versus EBERs-positive HK1 cell lines We established stable transfection of EBERs in the EBV-negative NPC cell line, HK1,to elucidate the role of the EBERs in NPC pathogenesis. Microarray gene expression profiling was carried out to investigate candidate genes which expression correlates with the expression of the EBERs. Total RNA was extracted from each cell line and processed using GeneChipÂ® Whole Transcript (WT) Sense Target Labelling Assay and then analyzed with GeneChipÂ® Human Gene 1.0 ST Array, with three repeats. Candidate genes differentially expressed between the two transfected HK1 cell lines were identified using GeneSpring GX 10 (Agilent Technologies).

2012-12-31 | E-GEOD-29123 | biostudies-arrayexpress

Comparative gene expression analysis upon stimulation of the human BCR or an inducible LMP2A in EBV immortalized lymphoblastoid cell lines

Project description:Survival of all B cells depends on signals from the B-cell receptor (BCR). In BCRnegative B cells the latent membrane protein 2A (LMP2A) of Epstein-Barr virus (EBV) replaces this survival signal and might play a role in the development of EBV-positive Hodgkin lymphomas and posttransplantation lymphoproliferative disease. In these BCR-negative cells LMP2A provides a ‘tonic’ signal similar to BCR’s constitutive expression in the absence of antigen in order to maintain activating signaling pathways common to both receptor molecules. In most latently EBV-infected B cells LMP2A and BCR are co-expressed but it is largely unclear what LMP2A contributes with respect to B-cell activation, proliferation and viral latency in these BCR-positive cells. A common model suggests that LMP2A maintains herpesviral latency by blocking BCR-mediated signals but how LMP2A could serve both antithetical ends in BCRnegative and BCR-positive cells is elusive. Our comparative analysis of BCR and LMP2A now indicates that LMP2A is a true BCR mimic that dominates BCR-operated signaling pathways in EBV-infected, BCR-positive cells to provide activation signals, support stable infections in vivo and allow exit from latency. These findings suggest that LMP2A co-opts the situation in anergic B cells, where continuous BCR signaling results in maintenance of the anergic state accompanied by unresponsiveness to acute BCR stimulation. The microarray experiment was used to compare effects of BCR and LMP2A on gene expression regulation. EBV's LMP2A and the human BCR activate similar cellular target genes; some genes are regulated solely by BCR or LMP2A, no gene is counter regulated A 12 chip study using cDNA from three separate 2525 LMP2A knockout LCL cultures and three separate 3696.10 LMP2A:mCD69 LCL cultures; each culture tested before and after 90 min stimulation of the BCR and LMP2A:mCD69, respectively.

2011-01-01 | E-GEOD-25434 | biostudies-arrayexpress

Rewiring of B cell receptor signaling by Epstein-Barr virus LMP2A

Project description:Epstein-Barr virus (EBV) infects human B cells and reprograms them to allow virus replication and persistence. One key viral factor in this process is latent membrane protein 2A (LMP2A), which has been described as a B cell receptor (BCR) mimic promoting malignant transformation. However, how LMP2A signaling contributes to tumorigenesis remains elusive. By systematically comparing LMP2A and BCR signaling using quantitative phosphoproteomics and transcriptome profiling, we identified molecular mechanisms through which LMP2A affects B cell biology. Consistent with previous literature, we found that LMP2A mimics a subset of BCR signaling events, including tyrosine-phosphorylation of the kinase SYK, the calcium initiation complex consisting of BLNK, BTK, PLC2, and its downstream transcription factor NFAT. However, the vast majority of LMP2A-induced signaling events markedly differed from those induced by BCR stimulation. These included differential phosphorylation of kinases, phosphatases, adaptor proteins, transcription factors such as NFB and TCF3, as well as widespread changes in the transcriptional output of LMP2A-expressing B cells. LMP2A affected apoptosis and cell cycle checkpoints by dysregulating the expression of apoptosis regulators such as Bcl-xL and the tumor suppressor retinoblastoma-associated protein (RB1). Accordingly, LMP2A cooperated with drivers of Burkitt lymphoma, overexpressed MYC and an oncogenic cyclin D3 mutant, by counteracting the pro-apoptotic effects of MYC and by further inhibiting RB1 function to promote cell growth. Our results indicate that LMP2A rewires rather than mimics BCR signaling, promoting a signaling output that predisposes EBV-infected B cells to hyperproliferation and eventual malignant transformation.

2020-09-22 | PXD018566 | Pride

Transcriptome sequencing of nasopharyngeal carcinoma model system

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-02-05 | E-GEOD-54174 | biostudies-arrayexpress

Comparative gene expression analysis upon stimulation of the human BCR or an inducible LMP2A in EBV immortalized lymphoblastoid cell lines

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