SNAIL1 is involved in the control of the epithelial-mesenchymal transition in oral tongue squamous cell carcinoma
de Morais, Everton Freitas; Morais, Hannah Gil de Farias; de França, Glória Maria; Téo, Fábio Haach; Galvão, Hébel Cavalcanti; Salo, Tuula; Coletta, Ricardo D; Freitas, Roseana de Almeida (2023-02-01)
Elsevier
01.02.2023
De Morais, E. F., Morais, H. G. D. F., De França, G. M., Téo, F. H., Galvão, H. C., Salo, T., Coletta, R. D., & Freitas, R. D. A. (2023). SNAIL1 is involved in the control of the epithelial-mesenchymal transition in oral tongue squamous cell carcinoma. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology, 135(4), 530–538. https://doi.org/10.1016/j.oooo.2023.01.009
https://creativecommons.org/licenses/by-nc-nd/4.0/
© 2023. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.
https://creativecommons.org/licenses/by-nc-nd/4.0/
© 2023. This manuscript version is made available under the CC-BY-NC-ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.
https://creativecommons.org/licenses/by-nc-nd/4.0/
Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:oulu-202312133741
https://urn.fi/URN:NBN:fi:oulu-202312133741
Tiivistelmä
Abstract
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.
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.
Kokoelmat
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