<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ge J</submitter><funding>National “111” Project</funding><funding>Independent Exploration and Innovation Program of Central South University</funding><funding>Hunan Provincial Key Research and Development Program</funding><funding>Beijing Xisike Clinical Oncology Research Foundation</funding><funding>the scientific research program of FuRong laboratory</funding><funding>Natural Science Foundation of Hunan Province, China</funding><funding>The National Natural Science Foundation of China</funding><pagination>e010091</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11575282</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(11)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Nasopharyngeal carcinoma (NPC) is a distinct subtype of head and neck cancer which is prevalent in south of China and southeastern of Asia. Consistent activation of interferon (IFN) signaling, and impairment of T cell mediated antitumor immunity is frequent in NPC. Forkhead box A1 (FOXA1) is one of the earliest discovered pioneer factors, which can open up compact chromatin structures to facilitate the binding of other proteins to chromatin.&lt;h4>Methods&lt;/h4>By using RNA sequencing, it was discovered that FOXA1 suppresses the activation of the interferon signaling pathway and the expression of the related interferon-responsive genes in NPC cells. The effect of FOXA1 on programmed death-ligand 1 (PD-L1) expression in C666-1 and HK1 cells under conditions with or without IFN</pubmed_abstract><journal>Journal for immunotherapy of cancer</journal><pubmed_title>FOXA1 enhances antitumor immunity via repressing interferon-induced PD-L1 expression in nasopharyngeal carcinoma.</pubmed_title><pmcid>PMC11575282</pmcid><funding_grant_id>82072596</funding_grant_id><funding_grant_id>2022SK2026</funding_grant_id><funding_grant_id>82173339</funding_grant_id><funding_grant_id>No.2023SK2094</funding_grant_id><funding_grant_id>82272631</funding_grant_id><funding_grant_id>1053320221155</funding_grant_id><funding_grant_id>YHR2020ZD-0052</funding_grant_id><funding_grant_id>2024JJ3036</funding_grant_id><funding_grant_id>No. Project #111-2-12</funding_grant_id><funding_grant_id>U23A20456</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Xiang B</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Chen P</pubmed_authors><pubmed_authors>Yi M</pubmed_authors><pubmed_authors>Zeng Z</pubmed_authors><pubmed_authors>Ge J</pubmed_authors><pubmed_authors>Xiong W</pubmed_authors></additional><is_claimable>false</is_claimable><name>FOXA1 enhances antitumor immunity via repressing interferon-induced PD-L1 expression in nasopharyngeal carcinoma.</name><description>&lt;h4>Background&lt;/h4>Nasopharyngeal carcinoma (NPC) is a distinct subtype of head and neck cancer which is prevalent in south of China and southeastern of Asia. Consistent activation of interferon (IFN) signaling, and impairment of T cell mediated antitumor immunity is frequent in NPC. Forkhead box A1 (FOXA1) is one of the earliest discovered pioneer factors, which can open up compact chromatin structures to facilitate the binding of other proteins to chromatin.&lt;h4>Methods&lt;/h4>By using RNA sequencing, it was discovered that FOXA1 suppresses the activation of the interferon signaling pathway and the expression of the related interferon-responsive genes in NPC cells. The effect of FOXA1 on programmed death-ligand 1 (PD-L1) expression in C666-1 and HK1 cells under conditions with or without IFN</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2025-04-04T20:38:59.069Z</modification><creation>2025-04-04T20:38:59.069Z</creation></dates><accession>S-EPMC11575282</accession><cross_references><pubmed>39542656</pubmed><doi>10.1136/jitc-2024-010091</doi></cross_references></HashMap>