ArticleOncology research2024
The Epstein-Barr virus-miRNA-BART6-5p regulates TGF-β/SMAD4 pathway to induce glycolysis and enhance proliferation and metastasis of gastric cancer cells.
Article in Oncology research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- EBV-HSA-RegDB: A database of regulatory interactions between Epstein-Barr virus and human miRNAs.Archives of virology · 2026Article
- Glycolysis‑driven immunosuppression in gastric cancer: Metabolic crosstalk between tumor cells and the immune microenvironment (Review).International journal of oncology · 2026Review
- Bioinformatics-driven genome-wide identification of viral miRNAs in high spillover bat coronaviruses and their target genes in human.Archives of microbiology · 2026Article
- Research progress on the mechanisms of EB virus reshaping the immune microenvironment in nasopharyngeal carcinoma.Clinical and experimental medicine · 2026Review
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- EBV-miR-BART14-3p Targets LACTB to Enhance Gastric Cancer Cell Proliferation and Migration.Biochemical genetics · 2026Article
- PIK3R1 as a Gastric Cancer Biomarker Linked to CD73Oncology research · 2026Article
- EBV-Derived miR-BART20-3p Influences Proliferation and Migration in EBV-Positive Gastric Cancer Models by Suppressing PPARα.Microorganisms · 2025Article
- Harnessing glycolysis in gastric cancer: molecular targets, therapeutic strategies, and clinical horizons.Frontiers in immunology · 2025Review
- Advances in glycolysis research in gastric cancer: molecular mechanisms, regulatory networks, and therapeutic potential.Frontiers in oncology · 2025Review
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6 authors.
Funding
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Abstract
Background: EBV-miR-BARTs exhibit significant relevance in epithelial tumors, particularly in EBV-associated gastric and nasopharyngeal cancers. However, their specific mechanisms in the initiation and progression of gastric cancer remain insufficiently explored. Material and Methods: Initially, EBV-miRNA-BART6-5p and its target gene SMAD4 expression were assessed in EBV-associated gastric cancer tissues and cell lines. Subsequent transfection induced overexpression of EBV-miRNA-BART6-5p in AGS and MKN-45, and downregulation in EBV-positive cells (SUN-719). The subsequent evaluation aimed to observe their impact on gastric cancer cell proliferation, migration, and glycolytic processes, with the TGF-β/SMAD4 signaling pathway value clarified using a TGF-β inhibitor. Results: EBV-miRNA-BART6-5p exhibits pronounced upregulation in EBV-associated gastric cancer tissues and EBV-positive cells, while its target gene SMAD4 demonstrates downregulated expression. Upregulation of it can promote the proliferation and migration of gastric cancer cells. Additionally, We found EBV-miRNA-BART6-5p promotes glycolysis of gastric cancer cells. Inhibition of the TGF-β/SMAD4 signaling pathway resulted in suppressed proliferation and migration of gastric cancer cells, concomitant with a diminished glycolytic capacity. Conclusion: In this study, we found that EBV-miRNA-BART6-5p can target SMAD4, effectively increasing glycolysis in gastric cancer cells by regulating the TGF-β/SMAD4 signaling pathway, thereby enhancing the proliferation and metastasis of gastric cancer cells. Our findings may offer new insights into the metabolic aspects of gastric cancer.
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