ArticleFrontiers in pharmacology2025
ASF1B promotes gastric cancer progression by modulating H2AC20 and activating PI3K/AKT and ERK1/2 pathways.
Article in Frontiers in pharmacology, 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.
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Who cites it
2 citing papers in PubMed.
- Article
- Gastric cancer organoids: a promising model for personalized treatment of gastric cancer.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Gastric cancer (GC) ranks among the most prevalent malignant neoplasms globally and is associated with a significant mortality rate. Despite the availability of various therapeutic interventions for GC, the overall prognosis for this disease remains unfavorable. This can be attributed to several factors, including delayed diagnosis and the inherent heterogeneity of the tumors. With the continuous enrichment of treatment methods, GC has entered an era of comprehensive treatment oriented toward precision and standardization. Methods: Through the application of bioinformatics and assessments of tissue microarrays, this study has selected the histone chaperone Anti-Silencing Function 1B (ASF1B) for detailed analysis, including clinical specimens. We then constructed ASF1B knockout and overexpression cell lines, and conducted biological function tests on this basis, validated at mouse and organoid levels. Additionally, human immunereconstitution was performed in NOD-PrkdcscidIl2rgem1/Smoc (NSG) mice, followed by flow cytometry analysis of mouse blood. Mechanically, protein-protein interaction analyses were conducted utilizing Immunoprecipitation-Mass Spectrometry (IP-MS) and Tandem mass tagging (TMT) methodologies to identify protein clusters. Results: The analysis demonstrated that ASF1B is significantly upregulated in GC tissues and correlates with unfavorable prognostic outcomes. Biological function tests provided that ASF1B contributes to tumor cell proliferation, colony formation, invasion and migration, and plays an important role in the progression of GC Conclusion: ASF1B, recognized as an oncogene, contributes to the initiation and progression of tumors, positioning it as a prospective target for therapeutic intervention in GC.
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