ArticleJournal for immunotherapy of cancer2025
EP300 compromises antitumor immunity by increasing SOCS1 expression.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- The expression landscape and clinical significance of cancer-specific RNA transcripts across human cancers.Journal of translational medicine · 2026Article
- Mechanism of action of alkaloids inOncology letters · 2026Article
- A Deep Learning-Generated Mixed Tumor-Stroma Ratio for Prognostic Stratification and Multi-omics Profiling in Bladder Cancer.Research (Washington, D.C.) · 2026Article
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13 authors.
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Abstract
backgroundBeyond supporting cancer cell proliferation, tumor growth relies on the ability of cancer cells to evade immune surveillance. Identifying novel molecules that promote tumor immune escape may help develop more effective immunotherapeutic strategies. The histone acetyltransferase E1A-binding protein p300 (EP300) is a key epigenetic regulator that modulates gene transcription through chromatin remodeling and acetylation of histones and transcription factors. However, its role in regulating immune evasion remains incompletely understood. This study investigates the impact of EP300 on tumor immune escape and suggests its potential as an immunotherapeutic target.
methodsWe analyzed tissue microarrays from patients with lung adenocarcinoma using immunohistochemistry to compare EP300 expression between cancerous tissues and benign tissues.
resultsEP300 was significantly upregulated in cancerous tissues compared with benign tissues. Genetic ablation of
conclusionsEP300 facilitates tumor immune evasion by suppressing antigen-presenting gene expression via SOCS1 upregulation. Our findings reveal a novel role for EP300 in mediating immune escape and propose a potential therapeutic strategy to enhance antitumor immunity.
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