Document Type : Original Article(s)
Authors
1 Dental Research Center, Oral Pathology Department, Dental Faculty, Hamadan University of Medical Sciences, Hamadan, Iran
2 Pathalogy Department, School of Medicine, Griffith University,Gold Coast, Australia
3 Department of Molecular Biology and Genetic Engineering, Stem Cell Technology Research Center, Tehran, Iran
Abstract
Background: Oral squamous cell carcinoma (OSCC) is the most common head and neck cancer with a continuing rise of incidence in developing countries. Despite the improvement in the clinical outcome of OSCC, the overall 5-year survival rate of patients is still disappointing. MicroRNAs (miRNAs) regulate gene expression in the post-transcriptional stage by targeting mRNAs. Advances in knowledge of the pathogenesis and molecular events lead to the improvement of OSCC treatments.
Materials and Methods: Human oral epidermoid carcinoma cells (KB), HGF1, and HEK 293T cell line were cultured. Lentiviral vectors were constructed and Western Blot analysis was performed. Then, immunocytochemistry staining was performed by using CD44 and vascular endothelial cadherin (VE-Cadherin) antibodies. All data were analyzed using the REST 2009 software. P values of ≤0.05 were considered statistically significant.
Results: MiR-143, miR-145, and miR 590 were down-regulated in the oral cancer cell line. Following transfection of Lv miR 143, Lv-miR-145, and Lv-miR-590, the expression of CD44 was markedly decreased in KB cells. In addition, transfection of miR-143 and miR- 590 mimics into the oral cancer cell line significantly decreased the expresion level of VE-Cadherin; however, transfection of miR-145 mimic had no significant effect on the expression of VE-Cadherin. Western blot analysis and immunocytochemistry staining confirmed the results.
Conclusion: This study revealed that miR-143, miR-145, and miR-590 negatively regulate CD44 and VE-Cadherin (except miR-145) expression, which might play a crucial role in the induction of cancer stem cells proliferation and angiogenesis in OSCC cells. The knowledge about the involved factors may provide new insights for the clinical use of miR- 143, mR-145, and miR-590 in the treatment of patients with OSCC.
Keywords
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