ArticleBMC cancer2020
Status of kinases in Epstein-Barr virus and Helicobacter pylori Coinfection in gastric Cancer cells.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 36 citations in OpenAlex.
- The research progress of the synergistic effect of Epstein-Barr virus andFrontiers in oncology · 2026Review
- Interplay of aurora kinase a functional residues and Epstein-barr Nuclear Antigen 1 in Epstein-barr virus associated Gastric cancer using AGS cells.BMC cancer · 2025Article
- Association ofFrontiers in medicine · 2025Review
- Gut-brain axis interplay via STAT3 pathway: Implications ofVirulence · 2024Article
- The role ofHeliyon · 2024Article
- Helicobacter pylori and Epstein-Barr virus infection in cell polarity alterations.Folia microbiologica · 2024Review
- Aurora Kinase A: Integrating Insights into Cancer, Inflammation, and Infectious Diseases.Gut microbes reports · 2024Review
- Implications of lncRNAs inFrontiers in cellular and infection microbiology · 2024Review
- Gastric lymphoepithelial-like carcinoma presenting as a sub-mucosal mass: a case report and literature review.American journal of translational research · 2023Article
- Article
- Kinases and therapeutics in pathogen mediated gastric cancer.Molecular biology reports · 2022Review
- Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.Current research in neurobiology · 2022Review
- Article
- Roles of Lytic Viral Replication and Co-Infections in the Oncogenesis and Immune Control of the Epstein-Barr Virus.Cancers · 2021Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHelicobacter pylori (H. pylori) and Epstein - Barr virus (EBV) plays a significant role in aggressive gastric cancer (GC). The investigation of genes associated with these pathogens and host kinases may be essential to understand the early and dynamic progression of GC.
aimThe study aimed to demonstrate the coinfection of EBV and H. pylori in the AGS cells through morphological changes, expression of the kinase and the probable apoptotic pathways.
methodsGenomic DNA isolation of H. pylori and its characterization from clinical samples were performed. RT-qPCR of kinases was applied to scrutinize the gene expression of kinases in co-infected GC in a direct and indirect (separated through insert size 0.45 μm) H. pylori infection set up. Morphological changes in co-infected GC were quantified by measuring the tapering ends of gastric epithelial cells. Gene expression profiling of apoptotic genes was assessed through RT-qPCR.
resultsAn interleukin-2-inducible T-cell kinase (ITK) showed significant upregulation with indirect H. pylori infection. Moreover, Ephrin type-B receptor six precursors (EPHB6) and Tyrosine-protein kinase Fyn (FYN) showed significant upregulation with direct coinfection. The tapering ends in AGS cells were found to be extended after 12 h. A total of 24 kinase genes were selected, out of which EPHB6, ITK, FYN, and TYK2 showed high expression as early as 12 h. These kinases may lead to rapid morphological changes in co-infected gastric cells. Likewise, apoptotic gene expression such as APAF-1 and Bcl2 family genes such as BAD, BID, BIK, BIM, BAX, AND BAK were significantly down-regulated in co-infected AGS cells.
conclusionAll the experiments were performed with novel isolates of H. pylori isolated from central India, for the functional assessment of GC. The effect of coinfection with EBV was more profoundly observed on morphological changes in AGS cells at 12 h as quantified by measuring the tapering of ends. This study also identifies the kinase and apoptotic genes modulated in co-infected cells, through direct and indirect approaches. We report that ITK, EPHB6, TYK2, FYN kinase are enhanced, whereas apoptotic genes such as APAF-1, BIK, FASL, BAX are significantly down-regulated in AGS cells coinfected with EBV and H. pylori.
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