Journal
ORAL DISEASES
Volume 29, Issue 4, Pages 1495-1504Publisher
WILEY
DOI: 10.1111/odi.14143
Keywords
canine; DNA methylation; fascin1; MicroRNA-145; oral cancer; squamous cell carcinoma
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This study explored the significance of microRNA-145 (miR-145) and Fascin1 (FSCN1) in the invasion of canine oral squamous cell carcinoma (SCC). The results showed that miR-145 was downregulated while FSCN1 mRNA was upregulated in SCC tissues. Transfecting SCC cells with miR-145 or FSCN1 siRNA inhibited cell growth and attenuated cell migration and invasion by inhibiting epithelial-to-mesenchymal transition. Furthermore, the promoter region of miR-145 was highly methylated in SCC cell lines and tissues.
Objectives Canine oral squamous cell carcinoma (SCC) often develops in the gingiva and tonsils. The biological behavior of canine oral SCC is similar to that of human head and neck SCC (HNSCC). Inhibiting invasion and metastasis is major importance for the treatment of canine and human HNSCC. In this study, the significance of microRNA (miR)-145 and Fascin1 (FSCN1) in the invasion of canine oral SCC was explored. Materials and methods Canine oral SCC tissues and cell lines were used for miR-145 and FSCN1 expression analysis via real-time PCR and immunohistochemistry. Canine oral SCC cell lines were used for in vitro assays. Results miR-145 was downregulated while FSCN1 mRNA was upregulated in canine oral SCC. Immunohistochemistry revealed that FSCN1 was upregulated in SCC when compared to normal mucosa. Transfection of canine SCC cells with miR-145 or FSCN1 siRNA suppressed cell growth and attenuated cell migration as well as invasion by inhibiting the epithelial-to-mesenchymal transition. Furthermore, the promoter region of miR-145 was highly methylated in SCC cell lines and tissues. Conclusion The expression profile and functions of miR-145 in canine oral SCC are similar to those in human HNSCC. Thus, canine oral SCC may represent a valuable preclinical model for human HNSCC.
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