DSCC1 serves as a prognostic correlate and promotes malignant progression in oral squamous cell carcinoma

While DSCC1 is overexpressed in several malignancies, its clinical relevance and biological function in oral squamous cell carcinoma (OSCC) remain incompletely characterized. DSCC1 expression in OSCC was analyzed using TCGA data. Associations with immune infiltration were inferred computationally. Functional assays were performed in CAL27 and SCC25 cells following DSCC1 knockdown and overexpression. Expression of cell cycle and signaling proteins was assessed by Western blotting. Candidate compounds were identified from the CTRP database, and the effect of KX2-391 on DSCC1 mRNA and protein levels was evaluated. DSCC1 was upregulated in OSCC, with expression increasing alongside advancing stage and grade. High DSCC1 expression correlated with poorer overall survival, disease-specific survival, and progression-free interval. Computational analyses suggested an inverse association between DSCC1 and effector immune cell signatures. DSCC1 knockdown suppressed OSCC cell proliferation, migration, and invasion, whereas overexpression promoted these phenotypes and was accompanied by increased CDK1, CDK6, PIK3CA, and phosphorylated mTOR protein levels. Among compounds examined, KX2-391 reduced DSCC1 mRNA and protein expression. DSCC1 is overexpressed in OSCC and correlates with adverse clinicopathological features and poor prognosis. It promotes malignant phenotypes in vitro, potentially involving modulation of cell cycle and PI3K/mTOR pathway components. KX2-391 suppresses DSCC1 expression and may serve as a pharmacological tool for further investigation of DSCC1-related biology.