AI Article Synopsis
- Oral squamous cell carcinoma (OSCC) is a highly prevalent cancer, especially in developing countries, with many patients experiencing relapse shortly after treatment, highlighting the need for new biomarkers for better survival.
- In laboratory experiments, exposure to arecoline significantly increased ZEB1 expression in oral epithelial cells, and reducing ZEB1 levels reversed its associated aggressive cancer traits such as increased migration and invasiveness.
- Clinically, higher ZEB1 levels were found in recurrent OSCC tumors compared to primary tumors, suggesting that ZEB1 could be a potential target for treatment and a marker for disease progression and recurrence in OSCC patients.
Article Abstract
Background: Oral squamous cell carcinoma (OSCC) is the sixth most prevalent malignancy worldwide and the third most common cancer in developing nation. Most OSCC patients relapse within months after receiving treatment. Therefore, searching the biomarkers of recurrence is urgently required to improve OSCC patient survival.
Methods: We set out to explore whether expression of ZEB1 could be triggered in oral epithelial cells (SG and FaDu) by arecoline in vitro. Control and ZEB1-knockdown arecoline-stimulated SG and FaDu were subjected to migration/invasiveness/anchorage-independent growth assay. Primary and recurrent OSCC tissues from areca quid chewers were analyzed using real-time RT-PCR analysis for ZEB1 expression.
Results: Arecoline led to dose-dependent elevation of ZEB1 expression in SG and FaDu cells. Downregulation of ZEB1 by lentiviral infection significantly reversed arecoline-induced oncogenicity including migration ability, cell invasiveness, and anchorage-independent growth in SG and FaDu cells. Clinically, the level of ZEB1 expression was higher in recurrent OSCC tumor samples but lower in primary lesions.
Conclusions: Targeting ZEB1 might offer a new strategy for the treatment of OSCC patients. ZEB1 can serve as a progression and relapse marker in OSCC patients.
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| http://dx.doi.org/10.1111/jop.12286 | DOI Listing |
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