Objective
The aim of the present study was to investigate the role of SNAIL1, E-cadherin, and
N-cadherin immunoexpression in oral tongue carcinogenesis. In addition, we evaluated
in vitro the impact of silencing of the nuclear transcription factor SNAIL1 on the
viability, apoptosis, proliferation, migration, and invasion of SCC-9 and HSC-3 cells.
Study design
Immunohistochemical analysis of SNAIL1, E-cadherin, and N-cadherin was carried out
in 47 samples representing oral epithelial dysplasia (OED) and 41 oral tongue squamous
cell carcinoma (OTSCC). The suppression of SNAIL1 expression was performed using shRNA-expression
vectors in HSC-3 and SCC-9 cells to investigate in vitro the impact of SNAIL1 on proliferation,
apoptosis, viability, migration, and invasion of SCC-9 and HSC-3 cells.
Results
Significant differences were observed in the expression of SNAIL1, E-cadherin, and
N-Cadherin between OTSCC and OED. A low membrane expression of E-cadherin was strongly
associated with poor overall survival in patients with OTSCC (P < .05), but the association did not withstand the Cox multivariate survival analysis.
SNAIL1 silencing played a key role in the suppression of epithelial-mesenchymal transition
and inhibited migration and invasion of HSC-3 cells (P < .0001, P < .01, respectively). In SCC-9 cells, SNAIL1 silencing promoted a significant reduction
in the proliferation (P < .0001) and invasion (P < .0001).
Conclusions
The epithelial-mesenchymal transition is present in different stages of oral tongue
carcinogenesis, and SNAIL1 plays a key role in this process, although the underlying
mechanisms still need to be elucidated. Thus, SNAIL1 might be a promising therapeutic
target in OTSCC.
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Article info
Publication history
Published online: February 01, 2023
Accepted:
January 25,
2023
Received in revised form:
November 23,
2022
Received:
October 8,
2022
Publication stage
In Press Journal Pre-ProofIdentification
Copyright
© 2023 Elsevier Inc. All rights reserved.