SLUG is upregulated and induces epithelial mesenchymal transition in canine oral squamous cell carcinoma.
Shunsuke NoguchiKazuya HiranoNanami TanimotoTerumasa ShimadaHideo AkiyoshiPublished in: Veterinary and comparative oncology (2021)
SLUG, encoded by the Snai2 gene, is known to play a role in epithelial-mesenchymal transition (EMT), which contributes to cell invasion and metastasis in some types of human carcinomas. However, the mechanisms and roles of EMT in canine squamous cell carcinoma (SCC) have not yet been elucidated. We have previously established canine oral SCC cell lines, including tonsillar SCC, and in this study, we evaluated the effects of SLUG on the phenotypes regarding EMT of canine SCC cells. First, immunohistochemical analysis revealed that SLUG is upregulated in canine oral SCC tissues compared to that in non-tumoural oral mucosa. Furthermore, gain-of-function and loss-of-function of SLUG revealed that SLUG partly contributed to migration and invasion of cells, as well as the upregulation of EMT markers such as vimentin and SNAIL. Thus, the current study suggests that SLUG promotes cell migration and invasion through EMT induction in canine oral SCC, as well as human cancers.
Keyphrases
- epithelial mesenchymal transition
- signaling pathway
- transforming growth factor
- induced apoptosis
- squamous cell carcinoma
- endothelial cells
- single cell
- cell cycle arrest
- oxidative stress
- gene expression
- induced pluripotent stem cells
- pi k akt
- cell death
- poor prognosis
- radiation therapy
- copy number
- high grade
- dna methylation
- rectal cancer