Dataset Information

EBV proteomics data - Identification of Epstein-Barr Virus Replication Proteins in Burkitt's Lymphoma Cells

ABSTRACT: A SILAC based experiment of cells infected or uninfected with EBV

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): B Cell

DISEASE(S): Epstein-barr Virus Infectious Disease

SUBMITTER: David Matthews

LAB HEAD: David Matthews

PROVIDER: PXD002461 | Pride | 2015-11-06

REPOSITORIES: Pride

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Publications

Identification of Epstein-Barr Virus Replication Proteins in Burkitt's Lymphoma Cells.

Traylen Chris C Ramasubramanyan Sharada S Zuo Jianmin J Rowe Martin M Almohammad Rajaei R Heesom Kate K Sweet Steve M M SM Matthews David A DA Sinclair Alison J AJ

Pathogens (Basel, Switzerland) 20151029 4

The working model to describe the mechanisms used to replicate the cancer-associated virus Epstein-Barr virus (EBV) is partly derived from comparisons with other members of the Herpes virus family. Many genes within the EBV genome are homologous across the herpes virus family. Published transcriptome data for the EBV genome during its lytic replication cycle show extensive transcription, but the identification of the proteins is limited. We have taken a global proteomics approach to identify vir ...[more]

PMID: 26529022

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Project description:The better prognosis of patients with Epstein-Barr virus-positive gastric carcinoma than those with EBV-negative GC is correlated with the degree of recruitment of inflammatory tumor infiltrating cells (TIL) to the vicinity of tumor cells. We hypothesized that the better prognosis would associate with less genetic or epigenetic alterations in EBV(+)GC, or EBV infection should deregulate immune modulator proteins, of which secretion recruit TIL. Therefore we performed mRNA expression profilings in EBV(-)GC and EBV(+)GC, each of which was pair wise compared with their normal control. We found that EBV(+)GC had much more molecular homogeneity with focused alterations in immune modulator genes; The Pearson correlation matrix analyses demonstrated that EBV(+)GC tumor showed remarkably high tumor homogeneity. While EBV(-)GC had considerable number genes that are differentially expressed genes from their normal counterparts, EBV(+)GC showed only a handful, almost 20 fold less number of DEG than EBV(-)GC under the same p value cutoff (p<0.001). Gene ontology and pathway analyses showed that while pathways of cation homeostasis, digestion and ion transport were commonly deregulated in both GC types, genes for chromatin assembly, prostaglandin receptor activity, pattern specification process are selectively deregulated in EBV(-)GC tumors. In contrast, pathways or genes for cytokine activity, immune response and lipoprotein particle clearance are selectively deregulated in EBV(+)GC tumors. These results demonstrate that EBV(+)GC inherently evolves to high homogeneity with fewer changes in gene expression and these secret immune modulatory chemokines could recruit reactive immune cells to EBV(+)GC, leading to favorable microenvironment for cancer suppression. All patients underwent the surgery for advanced gastric carcinoma (GC) except one patient with early GC. The EBV-presence in the GC was verified by in situ EBV-encoded small RNA (ERER) staining.. The 14 paired EBV(-)GC patients and 12 paired EBV(+)GC patients were selected for this study. Tumor tissue (T)and normal tissues (N) from distant sites from tumor areas were dissected, frozen at -80C and were subjected to RNA purification, mRNA array profiling analyses.

Dataset Information

EBV proteomics data - Identification of Epstein-Barr Virus Replication Proteins in Burkitt's Lymphoma Cells

Publications

Identification of Epstein-Barr Virus Replication Proteins in Burkitt's Lymphoma Cells.

Similar Datasets

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