SPINK1 Facilitates Tumor Progression in OSCC: Insights from Single-cell RNA Sequencing

Objective This investigation aimed to delineate the role and underlying mechanism of Serine Peptidase Inhibitor Kazal Type 1 (SPINK1) in oral squamous cell carcinoma (OSCC) via single-cell RNA-seq data. Materials and Methods Subpopulations of OSCC cells were identified via the GEO database. Cell‒cell communication analysis, gene set variation analysis (GSVA), gene set enrichment analysis (GSEA), and miRNA network construction were used to evaluate the role of SPINK1 in OSCC. The expression profile of SPINK1 in OSCC was authenticated via immunohistochemistry, quantitative polymerase chain reaction (qPCR), and Western blotting. The tumorigenic propensity of SPINK1 was evaluated through overexpression and knockdown assays employing Cell Counting Kit-8 (CCK-8), scratch assays, and transwell assays. Results SPINK1 was closely associated with T cells, malignant cells, and an array of immune modulators, including chemokines and immunoinhibitors, throughout OSCC progression. SPINK1 operates through pathways involving P53 and WNT signalling cascades. Relative to their normal tissue counterparts, SPINK1 is upregulated in OSCC, resulting in increased cell proliferation, invasion, and migration upon SPINK1 overexpression, whereas SPINK1 knockdown has opposite effects. Conclusion SPINK1 has emerged as a promising therapeutic target for the management of OSCC, offering prospective avenues for tailored therapeutic interventions and precision medicine strategies.