Evidence map›Paper›PMID 42185863›Full record

ArticleClinical epigenetics2026

Arecoline-induced EV-mediated ZNF582 hypermethylation drives IFIT1-PD-L1 immune evasion in oral squamous cell carcinoma.

Hui-Hsin Ko, Hsin-Hui Peng, Chun-Pin Chiang, Hsiang-Fong Kao, Hung-Ying Lin, Mark Yen-Ping Kuo, Shih-Jung Cheng

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Article in Clinical epigenetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Hui-Hsin KoGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Hsin-Hui PengGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Chun-Pin ChiangGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Hsiang-Fong KaoDepartment of Medical Oncology, National Taiwan University Cancer Center, Taipei, Taiwan.
Hung-Ying LinGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Mark Yen-Ping KuoGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.
Shih-Jung ChengGraduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan. sjcheng56@ntu.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study examined the role of arecoline-induced zinc finger protein 582 (ZNF582) methylation via extracellular vesicles (EVs) in oral squamous cell carcinoma (OSCC) and its effect on PD-L1 expression through the interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) pathway. MATERIALS AND

methodsEVs were isolated from SAS and TW2.6 cancer cell lines using ultracentrifugation and characterized using electron microscopy. ZNF582 methylation and protein expression were assessed, with stemness and epithelial-mesenchymal transition (EMT) markers analyzed via Western blotting. T cell populations were evaluated using flow cytometry.

resultsArecoline-induced ZNF582 methylation via EVs reduced protein expression. ZNF582 knockdown promoted OSCC proliferation, migration, stemness, and EMT, and increased PD-L1 expression, aiding immune evasion via IFIT1. PD-L1 expression was linked to lower CD4+/CD8 + T cell ratios in OSCC patients.

conclusionArecoline-induced ZNF582 hypermethylation via EVs promotes immune evasion through IFIT1, suggesting a potential therapeutic target for OSCC treatment. CLINICAL RELEVANCE: Targeting the EV-mediated ZNF582-IFIT1-PD-L1 pathway may offer new therapeutic strategies for immune modulation in OSCC patients, especially those with a history of areca nut exposure.

Indexed as

ArecolineCarcinoma, Squamous CellDNA MethylationExtracellular VesiclesImmune EvasionKruppel-Like Transcription FactorsMouth NeoplasmsAdaptor Proteins, Signal TransducingB7-H1 AntigenCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell Line, TumorEpithelial-Mesenchymal TransitionFemaleHumansMaleAdaptor Proteins, Signal TransducingArecolineB7-H1 AntigenCD274 protein, humanIFIT1 protein, humanKruppel-Like Transcription FactorsRNA-Binding ProteinsZNF582 protein, humanArecolineExtracellular vesicles (EVs)IFIT1Oral squamous cell carcinoma (OSCC)PD-LZNF582

Identifiers

PMID42185863
PMCPMC13202916

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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.