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Around half of all patients with oral squamous cell carcinoma (OSCC) present with lymphatic metastasis, a strong predictor of poor survival. Improving survival rates depends on preventing the first step in the "invasion - metastasis cascade," epithelial - to - mesenchymal transition (EMT), and developing antilymphangiogenesis therapies that antagonize lymphatic metastasis. The extracellular matrix - related protein WISP - 1 (WNT1 - inducible signaling pathway protein - 1) stimulates bone remodeling and tumor progression. We have previously reported that WISP - 1 promotes OSCC cell migration and lymphangiogenesis induced by vascular endothelial growth factor C (VEGF - C). This investigation sought to determine the role of WISP - 1 in regulating EMT in OSCC. Our analysis of oral cancer data from The Cancer Genome Atlas (TCGA) database revealed significant and positive associations between levels of WISP - 1 expression and clinical disease stage, as well as regional lymph node metastasis. We also found higher levels of WISP - 1 expression in serum samples obtained from patients with OSCC compared with samples from healthy controls. In a series of in vitro investigations, WISP - 1 activated EMT signaling via the FAK/ILK/Akt and Snail signaling transduction pathways and downregulated miR - 153 - 3p expression in OSCC cells. Our findings detail how WISP - 1 promotes EMT via the miR - 153 - 3p/Snail axis in OSCC cells.

WISP-1 Promotes Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma Cells via the miR-153-3p/Snail Axis