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Quantifying Antibody-Dependent Cellular Cytotoxicity in a Tumor Spheroid Model: Application for Drug Discovery
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EP300 compromises antitumor immunity by increasing SOCS1 expression.

Yanqiong Zeng1, Ying Zhou1,2, Jiayin Ruan1

  • 1National Key Laboratory of Immunity and Inflammation, Suzhou Institute of Systems Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Suzhou, Jiangsu, China.

Journal for Immunotherapy of Cancer
|October 15, 2025
PubMed
Summary
This summary is machine-generated.

The histone acetyltransferase EP300 (E1A-binding protein p300) promotes tumor immune escape by upregulating SOCS1, which suppresses antigen presentation. Inhibiting EP300 may enhance antitumor immunity by increasing CD8+ T cell infiltration.

Keywords:
ImmunotherapyJAK-STATMajor histocompatibility complex - MHCTumor microenvironment - TME

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Area of Science:

  • Cancer immunology
  • Epigenetics
  • Tumor microenvironment

Background:

  • Tumor growth depends on immune evasion.
  • EP300 (E1A-binding protein p300) is an epigenetic regulator.
  • EP300's role in immune evasion is unclear.

Purpose of the Study:

  • Investigate EP300's impact on tumor immune escape.
  • Determine EP300's potential as an immunotherapeutic target.

Main Methods:

  • Analyzed EP300 expression in lung adenocarcinoma tissues.
  • Generated Ep300-knockout cancer cells using CRISPR-Cas9.
  • Assessed tumor growth and CD8+ T cell infiltration in vivo.
  • Utilized RNA sequencing, ChIP sequencing, flow cytometry, and western blot to explore mechanisms.

Main Results:

  • EP300 was upregulated in cancerous tissues.
  • Ep300 ablation suppressed tumor growth and increased CD8+ T cell infiltration.
  • EP300 upregulates SOCS1, inhibiting STAT1 phosphorylation and antigen-presenting genes.

Conclusions:

  • EP300 facilitates immune evasion by suppressing antigen presentation via SOCS1.
  • EP300 plays a novel role in immune escape.
  • EP300 is a potential therapeutic target to enhance antitumor immunity.