Oral squamous cell carcinoma (OSCC) is a disfiguring malignancy and significantly impacts the quality of patient's life. Kallikrein-related peptidase 4 (KLK4), which is closely related to cancers, is highly expressed in OSCC. To explore the biological function of KLK4 in OSCC, a KLK4-specific shRNA was used to silence its endogenous expression, and then the migration and invasion of OSCC cells were explored. Results of our study showed that silencing KLK4 inhibited the migration and invasion of OSCC cells. The protein levels of epithelial mesenchymal transition-associated markers and proteases were also altered by KLK4 silencing. Further study showed that the phosphatidylinositol 3-kinase (PI3 K)/protein kinase B (AKT) signaling pathway was involved in the function of KLK4. Treatment with a PI3 K/AKT activator reversed the migration-inhibitory effect of KLK4 shRNA. Our study suggests that KLK4 may contribute to the metastasis of OSCC through the PI3 K/AKT signaling pathway.
Keywords: KLK4; OSCC; PI3 K/AKT; invasion; migration.