EP300 compromises antitumor immunity by increasing SOCS1 expression.

ABSTRACT:

Background

Beyond 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.

Methods

We analyzed tissue microarrays from patients with lung adenocarcinoma using immunohistochemistry to

SUBMITTER: Zeng Y 

PROVIDER: S-EPMC12530425 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature