Differential Transcriptomic Signatures of Oral Squamous Cell Carcinoma Compared with Normal Oral Epithelium
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Oral squamous cell carcinoma (OSCC) is the most prevalent malignant tumor of the oral cavity and is characterized by extensive genetic and phenotypic alterations during its development and progression. To better understand the transcriptomic landscape associated with OSCC, we performed a comparative analysis using a publicly available microarray dataset (GSE30784) comprising OSCC and normal oral epithelial tissues. Dimensionality-reduction analyses, including principal component analysis (PCA), t-distributed stochastic neighbor embedding (t-SNE), and uniform manifold approximation and projection (UMAP), demonstrated clear separation between OSCC and normal samples, indicating distinct global transcriptional patterns. Differential expression analysis identified a large number of significantly altered genes, among which extracellular matrix (ECM) remodeling–related genes such as COL1A1, COL1A2, COL4A1, COL4A2, ADAMTS2, MMP1, and GREM1 were markedly upregulated in OSCC. In contrast, genes associated with epithelial integrity or metabolic homeostasis, including ATP6V0A4, LOC284825, and AGFG2, were downregulated. A heatmap of the top 20 differentially expressed genes revealed clear clustering of OSCC versus normal tissues, reaffirming substantial transcriptional divergence between the two groups. Gene Ontology (GO) enrichment analysis showed that upregulated genes were predominantly involved in extracellular matrix organization, collagen fibril formation, and immune cell chemotaxis, suggesting extensive ECM remodeling and inflammatory microenvironment activation in OSCC. Downregulated genes were enriched in epidermis development, keratinocyte differentiation, and cytoskeletal organization, reflecting loss of epithelial identity and structural disruption. KEGG pathway analysis further highlighted the involvement of ECM–receptor interaction, focal adhesion, PI3K–Akt signaling, and cytokine–cytokine receptor interaction in OSCC pathogenesis. Overall, this study provides a comprehensive overview of transcriptomic alterations in OSCC by integrating global expression patterns, differential gene profiling, and functional pathway analysis. These findings contribute to a deeper understanding of the molecular characteristics of OSCC and offer foundational insights for the discovery of potential diagnostic markers or therapeutic targets.
Abstract
Oral squamous cell carcinoma (OSCC) is the most prevalent malignant tumor of the oral cavity and is characterized by extensive genetic and phenotypic alterations during its development and progression. To better understand the transcriptomic landscape associated with OSCC, we performed a comparative analysis using a publicly available microarray dataset (GSE30784) comprising OSCC and normal oral epithelial tissues. Dimensionality-reduction analyses, including principal component analysis (PCA), t-distributed stochastic neighbor embedding (t-SNE), and uniform manifold approximation and projection (UMAP), demonstrated clear separation between OSCC and normal samples, indicating distinct global transcriptional patterns. Differential expression analysis identified a large number of significantly altered genes, among which extracellular matrix (ECM) remodeling–related genes such as COL1A1, COL1A2, COL4A1, COL4A2, ADAMTS2, MMP1, and GREM1 were markedly upregulated in OSCC. In contrast, genes associated with epithelial integrity or metabolic homeostasis, including ATP6V0A4, LOC284825, and AGFG2, were downregulated. A heatmap of the top 20 differentially expressed genes revealed clear clustering of OSCC versus normal tissues, reaffirming substantial transcriptional divergence between the two groups. Gene Ontology (GO) enrichment analysis showed that upregulated genes were predominantly involved in extracellular matrix organization, collagen fibril formation, and immune cell chemotaxis, suggesting extensive ECM remodeling and inflammatory microenvironment activation in OSCC. Downregulated genes were enriched in epidermis development, keratinocyte differentiation, and cytoskeletal organization, reflecting loss of epithelial identity and structural disruption. KEGG pathway analysis further highlighted the involvement of ECM–receptor interaction, focal adhesion, PI3K–Akt signaling, and cytokine–cytokine receptor interaction in OSCC pathogenesis. Overall, this study provides a comprehensive overview of transcriptomic alterations in OSCC by integrating global expression patterns, differential gene profiling, and functional pathway analysis. These findings contribute to a deeper understanding of the molecular characteristics of OSCC and offer foundational insights for the discovery of potential diagnostic markers or therapeutic targets.