University of Oulu

de Morais, EF, de Farias Morais, HG, de Moura Santos, E, et al. TWIST1 regulates proliferation, migration, and invasion and is a prognostic marker for oral tongue squamous cell carcinoma. J Oral Pathol Med. 2022; 1- 9. doi:10.1111/jop.13377

TWIST1 regulates proliferation, migration, and invasion and is a prognostic marker for oral tongue squamous cell carcinoma

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Author: de Morais, Everton Freitas1; de Farias Morais, Hannah Gil1; de Moura Santos, Edilmar1;
Organizations: 1Federal University of Rio Grande do Norte, Natal, Brazil
2Department of Oral Diagnosis, School of Dentistry, University of Campinas (UNICAMP), Piracicaba, Brazil
3Cancer and Translational Medicine Research Unit, Faculty of Medicine and Medical Research Center Oulu, Oulu University Hospital, University of Oulu, Oulu, Finland
4Department of Pathology, Helsinki University Hospital, Institute of Oral and Maxillofacial Disease, University of Helsinki, and HUSLAB, Helsinki, Finland
5School of Dentistry, University of Campinas, Piracicaba, Brazil
Format: article
Version: accepted version
Access: embargoed
Persistent link: http://urn.fi/urn:nbn:fi-fe2022122173018
Language: English
Published: John Wiley & Sons, 2022
Publish Date: 2023-11-07
Description:

Abstract

Background: Epithelial–mesenchymal transition is one of the main mechanisms for tumor progression and metastasis. Transcription factors such as TWIST1 are key regulators of the epithelial–mesenchymal transition and are regarded as potential therapeutic targets for the treatment of cancer. The purpose of this study was to examine TWIST1 as a possible epithelial-mesenchymal transition-related prognostic biomarker in oral epithelial dysplasia and oral tongue squamous cell carcinomas, as well as the biological behavior of TWIST1-silencing in oral tongue squamous cell carcinomas cell lines.

Methods: Immunohistochemical analysis of TWIST1, E-cadherin, and N-cadherin was carried out in 47 samples representing oral epithelial dysplasia and 41 oral tongue squamous cell carcinomas. The suppression of TWIST1 expression was performed using shRNA-expression vectors in HSC-3 and SCC-9 cells to investigate in vitro the impact of TWIST1 on proliferation, apoptosis, viability, migration, and invasion of SCC-9 and HSC-3 cells.

Results: The expression of nuclear TWIST1 was significantly higher in oral tongue squamous cell carcinomas than in oral epithelial dysplasis (p < 0.0001), whereas TWIST1 in the cytoplasm was more expressed in oral epithelial dysplasis (p = 0.012). The high cytoplasmic expression of TWIST1 was significantly associated with shortened overall survival (p < 0.05), and increased nuclear TWIST1 expression was significantly related to high risk of recurrence (p = 0.03). Knockdown of TWIST1 in oral tongue squamous cell carcinomas cells induced the expression of E-cadherin and inhibited N-cadherin, which were followed by decreased proliferation, migration, and invasion.

Conclusions: Our research suggests that TWIST1 is linked to the development of oral tongue carcinogenesis and may be used as a prognostic indicator and therapeutic target for oral tongue squamous cell carcinomas patients.

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Series: Journal of oral pathology & medicine
ISSN: 0904-2512
ISSN-E: 1600-0714
ISSN-L: 0904-2512
Issue: Online first
DOI: 10.1111/jop.13377
OADOI: https://oadoi.org/10.1111/jop.13377
Type of Publication: A1 Journal article – refereed
Field of Science: 3122 Cancers
Subjects:
Funding: Conselho Nacional de Desenvolvimento Científico e Tecnológico; Coordenação de Aperfeiçoamento de Pessoal de Nível Superior; Universidade Federal do Rio Grande do Norte
Copyright information: © 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. This is the peer reviewed version of the following article: de Morais, EF, de Farias Morais, HG, de Moura Santos, E, et al. TWIST1 regulates proliferation, migration, and invasion and is a prognostic marker for oral tongue squamous cell carcinoma. J Oral Pathol Med. 2022; 1- 9, which has been published in final form at http://dx.doi.org/10.1111/jop.13377. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. This article may not be enhanced, enriched or otherwise transformed into a derivative work, without express permission from Wiley or by statutory rights under applicable legislation. Copyright notices must not be removed, obscured or modified. The article must be linked to Wiley’s version of record on Wiley Online Library and any embedding, framing or otherwise making available the article or pages thereof by third parties from platforms, services and websites other than Wiley Online Library must be prohibited.