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pmid:38355581

Recognizing the role of Epstein-Barr virus in gastric cancer: transcriptomic insights into malignancy modulation.

Tabassom Sedaghat Anbouhi · Hossein Sazegar · Ebrahim Rahimi

Virology journal · 2024 doi:10.1186/s12985-024-02307-z

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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title
Recognizing the role of Epstein-Barr virus in gastric cancer: transcriptomic insights into malignancy modulation.
doi
10.1186/s12985-024-02307-z
pmid
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[0]
Tabassom Sedaghat Anbouhi
[1]
Hossein Sazegar
[2]
Ebrahim Rahimi
journal
Virology journal
year
2024
abstract
BACKGROUND: Studies show that Epstein-Barr virus (EBV) infection can play a role in malignancy and increase the risk of gastric cancer (GC). The objective of this research was to pinpoint genes whose expression may be influenced by EBV and play a role in the development of GC. METHODS: Candidate genes potentially susceptible to expression modulation in the presence of EBV were identified through the analysis of GSE185627 and GSE51575 datasets. The association of candidate genes with GC and the survival rate of patients was investigated based on the cancer genome atlas (TCGA) data. Also, pathways related to candidate genes were examined through the MsigDB database. The PPI network was used to identify Hub genes. To corroborate the obtained results, we utilized the RT-qPCR method, employing GC samples from both EBV + and EBV-cases, as well as adjacent normal samples. RESULTS: Our results showed that genes upregulated by the EBV in the GC cell line, as well as in EBV + samples, are significantly linked to pathways involving the immune response, inflammation, and the P53 pathway. Conversely, genes downregulated by EBV are closely linked to pathways involving cell proliferation and mTORC1. Examining the candidate genes revealed that a considerable portion of genes susceptible to downregulation under the influence of EBV exhibit oncogenic roles based on TCGA data. Moreover, some of these genes are associated with an unfavorable prognosis. Protein-protein interaction network analysis of candidate genes highlighted IFI44L and OAS2 as potential hub genes in the EBV-GC axis. Our RT-qPCR results further validated these findings, demonstrating that the expression levels of IFI44L and OAS2 were higher in EBV + samples compared to both healthy and EBV-samples. CONCLUSION: Our study underscores the capacity of EBV to exert regulatory control over genes associated with GC malignancy. In addition to its inflammatory effects, EBV elicits transcriptomic changes that appear to attenuate the progression of GC.
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Finally, using the Cox regression test, the relationship between the expression of candidate genes and the mortality rate of patients was evaluated.
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EBV-induced CXCL8 upregulation promotes vasculogenic mimicry in gastric carcinoma via NF-κB signaling
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mRNA Expression Profiling in EBV-postive Gastric Carcinoma and EBV-negative GC in comparison with their normal mucosa tissue
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borate the obtained results, we utilized the RT-qPCR method, employing GC samples from both EBV +
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potential hub genes in the EBV-GC axis. Our RT-qPCR results further validated these findings, de
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Complete file
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The objective of this research was to pinpoint genes whose expression may be influenced by EBV and play a role in the development of GC.\nMETHODS: Candidate genes potentially susceptible to expression modulation in the presence of EBV were identified through the analysis of GSE185627 and GSE51575 datasets. The association of candidate genes with GC and the survival rate of patients was investigated based on the cancer genome atlas (TCGA) data. Also, pathways related to candidate genes were examined through the MsigDB database. The PPI network was used to identify Hub genes. To corroborate the obtained results, we utilized the RT-qPCR method, employing GC samples from both EBV + and EBV-cases, as well as adjacent normal samples.\nRESULTS: Our results showed that genes upregulated by the EBV in the GC cell line, as well as in EBV + samples, are significantly linked to pathways involving the immune response, inflammation, and the P53 pathway. Conversely, genes downregulated by EBV are closely linked to pathways involving cell proliferation and mTORC1. Examining the candidate genes revealed that a considerable portion of genes susceptible to downregulation under the influence of EBV exhibit oncogenic roles based on TCGA data. Moreover, some of these genes are associated with an unfavorable prognosis. Protein-protein interaction network analysis of candidate genes highlighted IFI44L and OAS2 as potential hub genes in the EBV-GC axis. Our RT-qPCR results further validated these findings, demonstrating that the expression levels of IFI44L and OAS2 were higher in EBV + samples compared to both healthy and EBV-samples.\nCONCLUSION: Our study underscores the capacity of EBV to exert regulatory control over genes associated with GC malignancy. 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