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KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway
BACKGROUND: KIF18A has been shown to participate in the development of various human malignancies. However, the role of KIF18A in head and neck squamous cell carcinoma (HNSCC) remains unknown. This study investigated the function of KIF18A in HNSCC as well as its possible mechanisms. METHODS: In thi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798418/ https://www.ncbi.nlm.nih.gov/pubmed/35116978 http://dx.doi.org/10.21037/tcr.2019.09.38 |
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author | Liu, Guancheng Cai, Gengming He, Xiaosong Huang, Donghai Zhu, Gangcai Chen, Changhan Zhang, Xin |
author_facet | Liu, Guancheng Cai, Gengming He, Xiaosong Huang, Donghai Zhu, Gangcai Chen, Changhan Zhang, Xin |
author_sort | Liu, Guancheng |
collection | PubMed |
description | BACKGROUND: KIF18A has been shown to participate in the development of various human malignancies. However, the role of KIF18A in head and neck squamous cell carcinoma (HNSCC) remains unknown. This study investigated the function of KIF18A in HNSCC as well as its possible mechanisms. METHODS: In this study, we conducted in vitro experiments. First, we examined the effect of KIF18A on Tu686 and 6-10B cells via determining cell viability, colony formation ability and cell motility. And then, we examined that whether the carcinogenic effect of KIF18A is associated with Akt activation. RESULTS: Our current study demonstrated that KIF18A expression was increased in HNSCC patients and its cell lines. Knockdown and overexpression of KIF18A in HNSCC cells indicated that KIF18A promoted cancer cell proliferation, invasion and migration. Moreover, these bioactivity changes in HNSCC cells were accompanied by enhanced Vimentin expression and suppressed E-cadherin expression induced by KIF18A. Further mechanistic analysis revealed that the carcinogenic effect of KIF18A is associated with Akt activation, and blocking the activity of Akt reversed the malignant progression caused by KIF18A overexpression in HNSCC cells. CONCLUSIONS: Together, our study reveals that KIF18A accelerates the progression of HNSCC and that targeting KIF18A may be a potential therapeutic strategy for the HNSCC. |
format | Online Article Text |
id | pubmed-8798418 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87984182022-02-02 KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway Liu, Guancheng Cai, Gengming He, Xiaosong Huang, Donghai Zhu, Gangcai Chen, Changhan Zhang, Xin Transl Cancer Res Original Article BACKGROUND: KIF18A has been shown to participate in the development of various human malignancies. However, the role of KIF18A in head and neck squamous cell carcinoma (HNSCC) remains unknown. This study investigated the function of KIF18A in HNSCC as well as its possible mechanisms. METHODS: In this study, we conducted in vitro experiments. First, we examined the effect of KIF18A on Tu686 and 6-10B cells via determining cell viability, colony formation ability and cell motility. And then, we examined that whether the carcinogenic effect of KIF18A is associated with Akt activation. RESULTS: Our current study demonstrated that KIF18A expression was increased in HNSCC patients and its cell lines. Knockdown and overexpression of KIF18A in HNSCC cells indicated that KIF18A promoted cancer cell proliferation, invasion and migration. Moreover, these bioactivity changes in HNSCC cells were accompanied by enhanced Vimentin expression and suppressed E-cadherin expression induced by KIF18A. Further mechanistic analysis revealed that the carcinogenic effect of KIF18A is associated with Akt activation, and blocking the activity of Akt reversed the malignant progression caused by KIF18A overexpression in HNSCC cells. CONCLUSIONS: Together, our study reveals that KIF18A accelerates the progression of HNSCC and that targeting KIF18A may be a potential therapeutic strategy for the HNSCC. AME Publishing Company 2019-10 /pmc/articles/PMC8798418/ /pubmed/35116978 http://dx.doi.org/10.21037/tcr.2019.09.38 Text en 2019 Translational Cancer Research. 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/. |
spellingShingle | Original Article Liu, Guancheng Cai, Gengming He, Xiaosong Huang, Donghai Zhu, Gangcai Chen, Changhan Zhang, Xin KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title | KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title_full | KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title_fullStr | KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title_full_unstemmed | KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title_short | KIF18A promotes head and neck squamous cell carcinoma invasion and migration via activation of Akt signaling pathway |
title_sort | kif18a promotes head and neck squamous cell carcinoma invasion and migration via activation of akt signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8798418/ https://www.ncbi.nlm.nih.gov/pubmed/35116978 http://dx.doi.org/10.21037/tcr.2019.09.38 |
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