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MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process

BACKGROUND: The oncogene, malignant T-cell-amplified sequence 1 (MCTS1), has been found to be highly expressed in a variety of cancer cell lines. It has been shown to be involved in cell cycle progression and to confer a growth advantage for lymphomas and breast cancer. Nevertheless, the role of MCT...

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Autores principales: Huang, Zhexun, Su, Qiao, Li, Wuguo, Ren, Hui, Huang, Huiqiang, Wang, Anxun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: AME Publishing Company 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267330/
https://www.ncbi.nlm.nih.gov/pubmed/34277797
http://dx.doi.org/10.21037/atm-21-2361
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author Huang, Zhexun
Su, Qiao
Li, Wuguo
Ren, Hui
Huang, Huiqiang
Wang, Anxun
author_facet Huang, Zhexun
Su, Qiao
Li, Wuguo
Ren, Hui
Huang, Huiqiang
Wang, Anxun
author_sort Huang, Zhexun
collection PubMed
description BACKGROUND: The oncogene, malignant T-cell-amplified sequence 1 (MCTS1), has been found to be highly expressed in a variety of cancer cell lines. It has been shown to be involved in cell cycle progression and to confer a growth advantage for lymphomas and breast cancer. Nevertheless, the role of MCTS1 in contributing to the development of oral cancer remains elusive. METHODS: We analyzed the gene expression profiles of MCTS1 in normal oral keratinocytes and cancerous cells. Cellular proliferation, invasion, and migration experiments were performed to detect the effect of MCTS1 on the biological evolution of oral cancer. The in vitro results were verified by the in vivo lymphatic metastasis test. The underlying mechanism of MCTS1 in promoting oral cancer invasion and metastasis correlated with the epithelial-mesenchymal transition (EMT) process as revealed by western blotting. RESULTS: The results showed that MCTS1 was aberrantly expressed in oral cancer cells. MCTS1 overexpression significantly promoted tumor cell growth, proliferation, migration, and invasion. MCTS1-mediated lymphatic metastasis was verified in vivo using an intraplantar tumor model. Biomarkers associated with EMT progression were positively or negatively regulated upon knockdown or overexpression of MCTS1, respectively. CONCLUSIONS: Higher MCTS1 expression in oral cancer may be connected with an unfavorable prognosis due to involvement of MCTS1. MCTS1 potentiates the growth and proliferation of oral cancer cells and subsequent metastasis by regulating cell cycle and modifying the EMT process. KEYWORDS: Oral cancer; oncogene; malignant T-cell-amplified sequence 1 (MCTS1); metastasis; invasion
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spelling pubmed-82673302021-07-16 MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process Huang, Zhexun Su, Qiao Li, Wuguo Ren, Hui Huang, Huiqiang Wang, Anxun Ann Transl Med Original Article BACKGROUND: The oncogene, malignant T-cell-amplified sequence 1 (MCTS1), has been found to be highly expressed in a variety of cancer cell lines. It has been shown to be involved in cell cycle progression and to confer a growth advantage for lymphomas and breast cancer. Nevertheless, the role of MCTS1 in contributing to the development of oral cancer remains elusive. METHODS: We analyzed the gene expression profiles of MCTS1 in normal oral keratinocytes and cancerous cells. Cellular proliferation, invasion, and migration experiments were performed to detect the effect of MCTS1 on the biological evolution of oral cancer. The in vitro results were verified by the in vivo lymphatic metastasis test. The underlying mechanism of MCTS1 in promoting oral cancer invasion and metastasis correlated with the epithelial-mesenchymal transition (EMT) process as revealed by western blotting. RESULTS: The results showed that MCTS1 was aberrantly expressed in oral cancer cells. MCTS1 overexpression significantly promoted tumor cell growth, proliferation, migration, and invasion. MCTS1-mediated lymphatic metastasis was verified in vivo using an intraplantar tumor model. Biomarkers associated with EMT progression were positively or negatively regulated upon knockdown or overexpression of MCTS1, respectively. CONCLUSIONS: Higher MCTS1 expression in oral cancer may be connected with an unfavorable prognosis due to involvement of MCTS1. MCTS1 potentiates the growth and proliferation of oral cancer cells and subsequent metastasis by regulating cell cycle and modifying the EMT process. KEYWORDS: Oral cancer; oncogene; malignant T-cell-amplified sequence 1 (MCTS1); metastasis; invasion AME Publishing Company 2021-06 /pmc/articles/PMC8267330/ /pubmed/34277797 http://dx.doi.org/10.21037/atm-21-2361 Text en 2021 Annals of Translational Medicine. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Original Article
Huang, Zhexun
Su, Qiao
Li, Wuguo
Ren, Hui
Huang, Huiqiang
Wang, Anxun
MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title_full MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title_fullStr MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title_full_unstemmed MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title_short MCTS1 promotes invasion and metastasis of oral cancer by modifying the EMT process
title_sort mcts1 promotes invasion and metastasis of oral cancer by modifying the emt process
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8267330/
https://www.ncbi.nlm.nih.gov/pubmed/34277797
http://dx.doi.org/10.21037/atm-21-2361
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