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Transcriptomic Analysis Reveals Molecular Signatures Distinguishing Vocal Fold Leukoplakia from Benign Lesions: Synergistic Dysregulation of Chronic Inflammation, Immune Dysfunction, and Epithelial Barrier Disruption

ABSTRACT: Objective: Vocal cord leukoplakia (VCL) represents a precancerous laryngeal lesion with a risk of malignant transformation. By employing transcriptomic analysis, this research sought to ascertain the key signatures and regulatory networks capable of distinguishing VCL from benign lesions. Methods: Surgically resected tissues from 8 individuals with VCL and 11 individuals with vocal cord polyps (VCP) were included for RNA sequencing and bioinformatics analysis. Core genes were identified through differential expression analysis, and functional enrichment analyses were utilized to characterize the associated biological processes. Results: The transcriptomic profile of VCL was characterized by abnormalities in three primary aspects: activation of inflammation-related pathways (e.g., NF-κB), downregulation of immune function-related genes (e.g., CD8A, CD19), and downregulation of epithelial barrier-related molecules (e.g., CLDN4). Conclusion: The transcriptomic signatures of VCL are linked to the coordinated dysregulation of pathways related to inflammation, immunity, and the epithelial barrier.

ORGANISM(S): Homo sapiens

PROVIDER: GSE330007 | GEO | 2026/05/10

REPOSITORIES: GEO

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Project description:Vocal fold (VF) fibrosis, often caused by phonosurgery, radiation, or trauma, leads to irreversible voice dysfunction due to excessive ECM deposition and increased tissue stiffness. VF fibrosis, a significant cause of chronic dysphonia, lacks FDA-approved treatments, highlighting the critical need for novel antifibrotic therapeutic. TGF-β1 is a major driver in the pathological transformation of fibroblasts into contractile myofibroblasts in VF fibrosis via SMAD3, YAP1, and integrin signaling pathways. These pathways lead to increased ACTA2 expression, excessive collagen production, and progressive tissue stiffening. Leveraging the principle that local cells respond to tissue-specific signals, our ECM hydrogel derived from decellularized vocal fold lamina propria (VFLP-ECM) reduced ACTA2 expression in TGF-β1 stimulated vocal fold fibroblasts, showcasing antifibrotic potential. In this study, we evaluated the therapeutic potential of VFLP-ECM hydrogel in a rabbit VF injury model—treatment involved VFLP-ECM or bovine type I collagen injections into VFs 7 days after injury, with evaluations at 28 days post-injury. We compared two VFLP-ECM formulations: a manual process (VFLP (man)) and an accelerated automated method (VFLP (au)). VFLP (man) showed more modulated fibrosis-associated gene expressions when compared to VFLP (au) and collagen. Proteomic analysis revealed that VFLP (man) preserves a broader array of bioactive proteins, such as vitronectin, crucial in TGF-β1 signaling and ECM remodeling. The transcriptomic analysis uncovered a downregulation of key fibrotic markers and potential inhibition of regulators such as SMAD3, YAP1, and MRTFA, alongside the upregulation of SMAD7, an inhibitor of TGF-β signaling. Notably, treatment with VFLP (man) resulted in vocal folds with similar stiffness as uninjured controls, whereas tissues treated with collagen or VFLP (au) remained stiffer, indicating incomplete mechanical recovery. These data provide the first in vivo evidence that VFLP-ECM hydrogel—mainly when produced via manual decellularization—attenuates fibrosis by disrupting biochemical and biomechanical drivers of myofibroblast activation.

Dataset Information

Transcriptomic Analysis Reveals Molecular Signatures Distinguishing Vocal Fold Leukoplakia from Benign Lesions: Synergistic Dysregulation of Chronic Inflammation, Immune Dysfunction, and Epithelial Barrier Disruption

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