OVOL1 inhibits oral squamous cell carcinoma growth and metastasis by suppressing zinc finger E-box binding homeobox 1.
| Autor: | Xu C; Department of Experimental Orofacial Medicine, Philipps University Marburg, Germany., Yan T; Department of Nanyuan Out-Patient, Affiliated Hospital of Stomatology, Nanjing Medical University, Jiangsu Key Laboratory of Oral Diseases Nanjing 210029, China., Yang J; Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, Jiangsu Key Laboratory of Oral Diseases Nanjing 210029, China. |
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| Jazyk: | angličtina |
| Zdroj: | International journal of clinical and experimental pathology [Int J Clin Exp Pathol] 2019 Jul 01; Vol. 12 (7), pp. 2801-2808. Date of Electronic Publication: 2019 Jul 01 (Print Publication: 2019). |
| Abstrakt: | Introduction: 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. Aims: To explore the roles of OVOL1 in the progression of OSCC, especially during metastasis. Results: 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. Conclusion: OVOL1 overexpression contributes to the progression of OSCC through inhibiting ZEB1, which may provide a marker for prognosis in OSCC. Competing Interests: None. (IJCEP Copyright © 2019.) |
| Databáze: | MEDLINE |
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