ArticleDrug design, development and therapy2025
ITGA4 Contributes to 5-Fluorouracil Resistance by Up-Regulating PI3K/AKT Signaling: Evidence from Network Pharmacology, Molecular Docking and Experimental Verification.
Article in Drug design, development and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- NR4A1 mediates chemotherapy‑induced senescence via the PI3K/AKT pathway in gastric cancer cells.Oncology reports · 2026Article
- Aronia Berry Extract Inhibits Cancer Stemness and Overcomes 5-Fluorouracil Resistance by Targeting TLR3/NF-κB Signaling in Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: 5-Fluorouracil (5-FU) is a mainstream drug used in chemotherapy and chemoradiotherapy regimens for the clinical treatment of malignancies, such as gastric cancer (GC), colorectal cancer, and breast cancer. However, the molecular mechanism of action of 5-FU in GC has not yet been studied using a network pharmacology approach. Methods: The mechanism of action of 5-FU in GC was determined using a network pharmacology technique, and our findings were confirmed by various computational approaches and experimental tests using the GeneCards database, ChEMBL database, STRING database, molecular docking, molecular dynamics simulation, DAVID, GEPIA, Kaplan‒Meier Plotter, CCK-8 assays, colony formation experiments, cell proliferative assay, apoptosis assays, wound-healing assays, Real-time PCR and Western blot tests. Results: A total of 21 shared and 13 potential targets were identified using PPI network analysis. Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analyses indicated that the PI3K/AKT signaling pathway may be a significant pathway. Combined with molecular docking and database verification, F10, NR3C1, DHFR, CA2, BCHE, ACHE, and ITGA4 were identified as candidate core genes. Moreover, the experimental results illustrated that ITGA4 induces 5-FU resistance by up-regulating PI3K/AKT signaling. Conclusion: Network pharmacology is a feasible scientific research strategy for revealing the multitarget-multipathway role of 5-FU in the treatment of GC and provides ITGA4-based new ideas and therapeutic strategy to overcome 5-FU resistance for GC treatment.
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Registered trials
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