ArticlePeerJ2025
Breaking epigenetic shackles: targeting ARID1A methylation and the PI3K/AKT/mTOR-PD-L1 axis to overcome immune escape in gastric cancer.
Article in PeerJ, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Multi Omics Integration in Colorectal Cancer: From Molecular Insights to Precision Oncology.Cancers · 2026Review
- Unveiling the Intricate Dance: Signaling Pathways in Liver Cancer Metabolism and Immunity.Current oncology reports · 2026Review
- Elucidating the dual regulation of apoptosis and migration by Ajugasterone C in AGS cells via the PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: AT-rich interaction domain 1A (ARID1A), is frequently mutated in cancer, leading to loss-of-function and posing challenges to therapeutic targeting. This study aimed to systematically explore epigenetic regulation of ARID1A, specifically promoter hypermethylation, in gastric cancer (GC) and its functional/immunological consequences. Methods: We employed multi-omics bioinformatics analyses (UALCAN, cBioPortal, MEXPRESS and UCSC Xena) combined with Results: Promoter hypermethylation was identified as a key mechanism silencing ARID1A transcriptional, showing a significant negative correlation between methylation Conclusion: ARID1A promoter hypermethylation drives an epigenetic-immune checkpoint cascade in GC. Combined with its association with immune signatures and PD-L1 upregulation, ARID1A hypermethylation emerges as a candidate biomarker for predicting immune checkpoint blockade (ICB) responsiveness and patient stratification in GC. Future studies should evaluate 5-aza-CdR-ICB-AKT inhibitor regimens in advanced models to guide clinical translation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.