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ABSTRACT Objective Methods Results Conclusions To investigate the cellular components and immunological characteristics of the head and neck rhabdomyosarcoma (RMS) microenvironment.We conducted single‐cell transcriptomics to analyze the cellular components of the RMS microenvironment. CellChat was utilized for analyzing intercellular interactions. The cancer genome atlas database was used for validation. CIBERSORT was applied for immune infiltration profiling. Functional enrichment analyses were performed using the Kyoto Encyclopedia of Genes and Genomes. Gene set scores were calculated using single‐sample gene set enrichment analysis. Subcutaneous allograft models and bulk RNA sequencing were used for validation. Flow cytometry and immunohistochemistry were used to identify M2‐like macrophages.Our findings revealed an extremely low presence of neutrophils in RMS samples compared with normal sample. RMS sample with high Schwann cell infiltration exhibited an increase in M2‐like macrophage infiltration. Receptor‐ligand pairs, specifically MIF‐CD74 and PTN‐SDC3, were identified between Schwann cells and M2‐like macrophages. In the RMS sample characterized by significant Schwann cell infiltration, M2‐like macrophages demonstrate robust expression of axon guidance factors and are enriched in the axon guidance pathway.Our study provides valuable insights into the microenvironment and immunological characteristics of RMS, offering crucial information for further research and potential therapeutic strategies. [ABSTRACT FROM AUTHOR]

Objective: Circular RNAs (CircRNAs) are involved in various tumors. However, their role in head and neck squamous cell carcinoma (HNSCC) is unknown. CircRNA sequencing data showed that hsa_circ_0000264 is significantly upregulated in HNSCC tissues. In this study, we aimed to investigate the role of hsa_circ_0000264 in HNSCC and elucidate its underlying regulation mechanism. Materials and Methods: RNase R treatment was performed to confirm the loop structure of hsa_circ_0000264. Fluorescence in situ hybridization was performed to show the subcellular localization of hsa_circ_0000264. We then performed wound healing assay, Transwell assay, Western blot, and in vivo experiments to determine the effect of alterations in hsa_circ_0000264 expression. We performed RNA pull‐down and dual luciferase reporter assay to identify and confirm the binding sites in RNAs. Results: hsa_circ_0000264 was upregulated in HNSCC tissues and cells, and its loop structure was confirmed. Knockdown of hsa_circ_0000264 inhibited the migration, invasion, and epithelial‐to‐mesenchymal transition of HNSCC cells in vivo and in vitro. Mechanistically, hsa_circ_000026 upregulation can upregulate the expression of high mobility group AT‐hook 2 (HMGA2) by sponging hsa‐let‐7b‐5p, which in turn promotes HNSCC progression. Conclusion: Our results showed that hsa_circ_0000264 promotes HNSCC progression via the hsa‐let‐7b‐5p/HMGA2 axis, and hsa_circ_0000264 can serve as a potential target for HNSCC treatment. [ABSTRACT FROM AUTHOR]

ObjectiveMaterials and MethodsResultsConclusionsTo investigate the mechanisms behind acquired resistance to erlotinib in head and neck squamous cell carcinoma (HNSCC) with a focus on the role of cancer‐associated fibroblasts (CAFs) and the PI3K/AKT signaling pathway.This study analyzed gene expression profiles of erlotinib‐sensitive and ‐resistant HNSCC cell lines using datasets from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. It included microarray and RNA‐sequencing data, differentially expressed genes (DEGs) analysis, and pathway enrichment. In vitro experiments assessed the functional role of CAFs and the impact of the extracellular matrix component COL5A2 on erlotinib resistance.We identified 124 DEGs associated with erlotinib resistance, with key genes like COL5A2 significantly upregulated. CAFs were found to highly express COL5A2, enhancing erlotinib resistance by activating the PI3K/AKT pathway. Higher erlotinib resistance scores correlated with increased infiltration of CAFs.Erlotinib resistance in HNSCC is significantly influenced by the tumor microenvironment (TME), particularly through CAFs and the PI3K/AKT pathway. Targeting these mechanisms may offer new therapeutic strategies to overcome resistance in HNSCC patients. [ABSTRACT FROM AUTHOR]