ArticleDiscover oncology2026
VAV2-associated ncRNA network in the focal adhesion pathway is dysregulated in laryngeal squamous cell carcinoma.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe focal adhesion is a key pathway for cellular proliferation and migration. This study aimed to elucidate the function of VAV2, a key guanine nucleotide exchange factor in the focal adhesion pathway, and to investigate its post-transcriptional relationships through the predicted VAV2/miRNA/lncRNA network in Laryngeal Squamous Cell Carcinoma (LSCC).
methodsRNA-seq data analysis from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets was performed using R software. Differential expression profiles of mRNAs, miRNAs, and lncRNAs were integrated with multi-database miRNA-target predictions to construct a high-confidence VAV2-associated ncRNA network. The RT-qPCR and Western blotting techniques were used to validate the gene analysis in 63 paired LSCC and adjacent normal tissues.
resultsFocal adhesion was among the significantly enriched pathways (47 genes, P = 2.23 × 10⁻⁴). VAV2 exhibited consistent upregulation at both mRNA and protein levels in tumor tissues (P < 0.0001). Tumor samples exhibited the downregulation of miR-449b-5p and miR-495-3p, along with pronounced significant overexpression of LINC00665 and CCDC144NL-AS1 (P < 0.01). Significant positive correlations were identified between VAV2 and lncRNAs (r = 0.76 and r = 0.79, P < 0.0001), alongside comparable negative correlations with miRNAs.
conclusionOur results proposed that the predicted VAV2-associated ncRNA network might be involved in the focal adhesion pathway. These data suggested novel insights into the underlying mechanisms and hold promise as biomarkers and therapeutic targets.
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