ArticleTranslational cancer research2022
Upregulated YTHDF1 associates with tumor immune microenvironment in head and neck squamous cell carcinomas.
Article in Translational cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- YTHDF1 Regulates RELA m6A Modification and Activates the NF-Kappa B Signaling Pathway to Promote the Mechanism of Gastric Cancer.Cancer medicine · 2025Article
- Prediction of neoadjuvant therapy efficacy in gastric cancer: the interplay between biomarkers and radiomics and its potential for clinical translation.Frontiers in oncology · 2025Review
- N6-methyladenosine RNA modification in head and neck squamous cell carcinoma (HNSCC): current status and future insights.Medical oncology (Northwood, London, England) · 2024Review
- High expression of ARPC1B correlates with immune infiltration and poor outcomes in glioblastoma.Biochemistry and biophysics reports · 2024Article
- Exploration of prognostic biomarkers in head and neck squamous cell carcinoma microenvironment from TCGA database.Annals of translational medicine · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
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Abstract
Background: The nature of the tumor immune microenvironment (TME) is essential for the head and neck squamous cell carcinomas (HNSCC) initiation, prognosis, and response to immunotherapy. However, its gene regulatory network remains to be elucidated. Methods: To identify N6-methyladenosine (m6A) regulators that are involved in regulating the HNSCC TME, a computational screen was applied to The Cancer Genome Atlas (TCGA) HNSCC patient samples. The effects of mutation, copy number variation (CNV), and transcriptional regulation on YTHDF1 expression were analyzed. We analyzed the TME infiltration, cancer-immunity cycle activities, and YTHDF1-related Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Results: Among the 24 m6A regulators, 3 factors (YTHDF1, ELAVL1, and METTL3) were highly correlated with TME infiltration. As the top candidate, YTHDF1 was up-regulated and amplified in HNSCC. YTHDF1 promoter gains active histone marks and high chromatin accessibility, which might be transcriptionally activated by SOX2 and TP63. Moreover, YTHDF1 expression significantly associates with tumor malignant phenotype in HNSCC, which has a positive correlation with CD4+ T cells and a negative correlation with CD8+ T cells infiltration. Specifically, YTHDF1 expression is negatively associated with the cancer-immunity cycle and immune checkpoint inhibitors. In terms of the underlying biological mechanisms, YTHDF1 may interact with YTHDF2/3 to regulate several vital immune-related pathways. Conclusions: We identify YTHDF1 associated with TME and elucidate an underlying mechanism of immune escape in HNSCC, which might be used as a predictive marker in guiding immunotherapy.
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