OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1

Lymph node metastasis is the primary cause of death in oral squamous-cell carcinoma (OSCC) patients, so understanding the underlying molecular mechanism is critical for treating metastatic OSCC. OVOL1, a transcription factor, functions as a "break" to repress metastasis in breast cancer and prostate cancer. To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis. The OVOL1 level was increased significantly in non-metastatic OSCC tissues and negatively correlated with ZEB1 level. OVOL1 repressed ZEB1 expression by directly binding to the promoter region of ZEB1. OVOL1 functioned as a tumor suppressor, and suppressed SCC-152 cells proliferation, migration, and invasion and promoted apoptosis. ZEB1 almost fully rescued the overexpressed OVOL1 function in SCC-152 cells. OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC.