ArticleJournal of experimental & clinical cancer research : CR2025
Myeloid cell-derived apCAFs promote HNSCC progression by regulating proportion of CD4
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed.
- Three-Year Follow-Up of Neoadjuvant Tislelizumab with Chemotherapy in Locally Advanced Gastric and Gastroesophageal Junction Adenocarcinoma: Revealing Cancer-Associated Fibroblast Heterogeneity Corresponding to PD-1 Blockade Efficacy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Trial
- Biomarkers Predictive of Immunotherapy Efficacy in Head and Neck Squamous Cell Carcinoma: Current Insights and Future Perspectives.World journal of otorhinolaryngology - head and neck surgery · 2026Review
- Cancer-associated fibroblasts as a target in head and neck squamous cell carcinoma: bridging mechanisms to therapy with drugs, adjuvants, and nanotechnology.Discover oncology · 2026Review
- Bidirectional crosstalk between cancer-associated fibroblasts and tumor immunity: shaping the microenvironment and response to immune checkpoint therapy.Experimental hematology & oncology · 2026Review
- Article
- Pancreatic ductal adenocarcinoma: integrating molecular insights for targeted interventions.Signal transduction and targeted therapy · 2026Review
- Decoding the CAF-TAM axis: multi-omics dissection and therapeutic targeting of stromal-immune crosstalk in the tumor microenvironment.Cell death & disease · 2026Review
- Mendelian Randomization and ScTranscriptomics Reveal a Lipid Low Malignant Cells Driving Immunosuppression and Matrix Remodeling in Oral squamous cell carcinoma.International dental journal · 2026Article
- Partial-EMT in oral squamous cell carcinoma: molecular circuitry and clinical translation.International journal of oral science · 2026Review
- Extracellular Matrix-Related Prognostic Signature for Head and Neck Squamous Cell Carcinoma via Multi-Algorithm Survival Modeling.Biomarker insights · 2026Article
- Cancer-Associated Fibroblast-Targeted Nanomedicine in Solid Tumor Therapy: From Mechanisms of Therapeutic Resistance to Precision Stromal Modulation.International journal of nanomedicine · 2026Review
- Unraveling the impact of cancer-associated fibroblasts on lymphatic metastasis of head and neck squamous cell carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Review
- CELLetter: leveraging large language model and dual-stream network to identify context-specific ligand-receptor interactions for cell-cell communication analysis.Briefings in bioinformatics · 2025Article
- Cancer-Associated Fibroblasts: Origin, Classification, Tumorigenicity, and Targeting for Cancer Therapy.MedComm · 2025Review
- Integrated single-cell and Mendelian randomization analyses: dissecting underlying causes of varied efficacy in immune neoadjuvant therapy for esophageal carcinoma.Discover oncology · 2025Article
- Cancer Risk in IBD Patients Treated with JAK Inhibitors: Reassuring Evidence from Trials and Real-World Data.Cancers · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well-known that cancer-associated fibroblasts (CAFs) are involved in the desmoplastic responses in Head and Neck Squamous Cell Carcinoma (HNSCC). CAFs are pivotal in the tumor microenvironment (TME) molding, and exert a profound influence on tumor development. The origin and roles of CAFs, however, are still unclear in the HNSCC, especially antigen-presenting cancer-associated fibroblasts (apCAFs). Our current study tried to explore the origin, mechanism, and function of the apCAFs in the HNSCC. Data from single-cell transcriptomics elucidated the presence of apCAFs in the HNSCC. Leveraging cell trajectory and Cellchat analysis along with robust lineage-tracing assays revealed that apCAFs were primarily derived from myeloid cells. This transdifferentiation was propelled by the macrophage migration inhibitory factor (MIF), which was secreted by tumor cells and activated the JAK/STAT3 signaling pathway. Analysis of the TCGA database has revealed that markers of apCAFs were inversely correlated with survival rates in patients with HNSCC. In vivo experiments have demonstrated that apCAFs could facilitate tumor progression. Furthermore, apCAFs could modulate ratio of CD4
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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.