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COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1
Collagen type IV α1 chain (COL4A1) is a collagen protein that acts as a tumor-promoting factor in several types of cancer. However, the role and the potential mechanisms involving COL4A1 in oral squamous cell carcinoma (OSCC) remain unclear. Using reverse transcription-quantitative PCR and western b...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10061039/ https://www.ncbi.nlm.nih.gov/pubmed/37006878 http://dx.doi.org/10.3892/etm.2023.11875 |
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author | Tian, Xiaobei Sun, Jian Li, Changshun Zhang, Kun |
author_facet | Tian, Xiaobei Sun, Jian Li, Changshun Zhang, Kun |
author_sort | Tian, Xiaobei |
collection | PubMed |
description | Collagen type IV α1 chain (COL4A1) is a collagen protein that acts as a tumor-promoting factor in several types of cancer. However, the role and the potential mechanisms involving COL4A1 in oral squamous cell carcinoma (OSCC) remain unclear. Using reverse transcription-quantitative PCR and western blotting, the expression levels of COL4A1 and (nidogen-1) NID1 in OSCC cells were assessed. Cell Counting Kit-8, EdU staining and colony formation assays were used to evaluate cell proliferation. Cell migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. The expression levels of proteins involved in epithelial-mesenchymal transition (EMT) were assessed using western blotting. In addition, the association between COL4A1 and NID1 was analyzed using TNMplot and the STRING database and verified by co-immunoprecipitation analysis. COL4A1 expression was found to be significantly increased in OSCC cells. Knockdown of COL4A1 expression decreased SCC-4 cell proliferation, migration and invasion, as well as the progression of EMT. In addition, COL4A1 was shown to be significantly positively associated with NID1 in OSCC and to bind to NID1. NID1 overexpression reversed the inhibitory effects of COL4A1 knockdown on cell proliferation, migration and invasion as well as on the progression of EMT in OSCC cells. In summary, the present findings demonstrated that COL4A1 promoted cell proliferation and migration as well as the progression of EMT in OSCC cells by binding to NID1, highlighting a potential avenue for therapeutic management of OSCC. |
format | Online Article Text |
id | pubmed-10061039 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-100610392023-03-31 COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 Tian, Xiaobei Sun, Jian Li, Changshun Zhang, Kun Exp Ther Med Articles Collagen type IV α1 chain (COL4A1) is a collagen protein that acts as a tumor-promoting factor in several types of cancer. However, the role and the potential mechanisms involving COL4A1 in oral squamous cell carcinoma (OSCC) remain unclear. Using reverse transcription-quantitative PCR and western blotting, the expression levels of COL4A1 and (nidogen-1) NID1 in OSCC cells were assessed. Cell Counting Kit-8, EdU staining and colony formation assays were used to evaluate cell proliferation. Cell migration and invasion were assessed using wound healing and Transwell invasion assays, respectively. The expression levels of proteins involved in epithelial-mesenchymal transition (EMT) were assessed using western blotting. In addition, the association between COL4A1 and NID1 was analyzed using TNMplot and the STRING database and verified by co-immunoprecipitation analysis. COL4A1 expression was found to be significantly increased in OSCC cells. Knockdown of COL4A1 expression decreased SCC-4 cell proliferation, migration and invasion, as well as the progression of EMT. In addition, COL4A1 was shown to be significantly positively associated with NID1 in OSCC and to bind to NID1. NID1 overexpression reversed the inhibitory effects of COL4A1 knockdown on cell proliferation, migration and invasion as well as on the progression of EMT in OSCC cells. In summary, the present findings demonstrated that COL4A1 promoted cell proliferation and migration as well as the progression of EMT in OSCC cells by binding to NID1, highlighting a potential avenue for therapeutic management of OSCC. D.A. Spandidos 2023-03-07 /pmc/articles/PMC10061039/ /pubmed/37006878 http://dx.doi.org/10.3892/etm.2023.11875 Text en Copyright: © Tian et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Tian, Xiaobei Sun, Jian Li, Changshun Zhang, Kun COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title | COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title_full | COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title_fullStr | COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title_full_unstemmed | COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title_short | COL4A1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to NID1 |
title_sort | col4a1 promotes the proliferation and migration of oral squamous cell carcinoma cells by binding to nid1 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10061039/ https://www.ncbi.nlm.nih.gov/pubmed/37006878 http://dx.doi.org/10.3892/etm.2023.11875 |
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