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BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9
BubR1 is a critical component of spindle assembly checkpoint, ensuring proper chromatin segregation during mitosis. Recent studies showed that BubR1 was overexpressed in many cancer cells, including oral squamous cell carcinomas (OSCC). However, the effect of BubR1 on metastasis of OSCC remains uncl...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4519889/ https://www.ncbi.nlm.nih.gov/pubmed/26151845 http://dx.doi.org/10.3390/ijms160715104 |
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author | Chou, Chou-Kit Wu, Chang-Yi Chen, Jeff Yi-Fu Ng, Ming-Chong Wang, Hui-Min David Chen, Jen-Hao Yuan, Shyng-Shiou F. Tsai, Eing-Mei Chang, Jan-Gowth Chiu, Chien-Chih |
author_facet | Chou, Chou-Kit Wu, Chang-Yi Chen, Jeff Yi-Fu Ng, Ming-Chong Wang, Hui-Min David Chen, Jen-Hao Yuan, Shyng-Shiou F. Tsai, Eing-Mei Chang, Jan-Gowth Chiu, Chien-Chih |
author_sort | Chou, Chou-Kit |
collection | PubMed |
description | BubR1 is a critical component of spindle assembly checkpoint, ensuring proper chromatin segregation during mitosis. Recent studies showed that BubR1 was overexpressed in many cancer cells, including oral squamous cell carcinomas (OSCC). However, the effect of BubR1 on metastasis of OSCC remains unclear. This study aimed to unravel the role of BubR1 in the progression of OSCC and confirm the expression of BubR1 in a panel of malignant OSCC cell lines with different invasive abilities. The results of quantitative real-time PCR showed that the mRNA level of BubR1 was markedly increased in four OSCC cell lines, Ca9-22, HSC3, SCC9 and Cal-27 cells, compared to two normal cells, normal human oral keratinocytes (HOK) and human gingival fibroblasts (HGF). Moreover, the expression of BubR1 in these four OSCC cell lines was positively correlated with their motility. Immunofluorescence revealed that BubR1 was mostly localized in the cytosol of human gingival carcinoma Ca9-22 cells. BubR1 knockdown significantly decreased cellular invasion but slightly affect cellular proliferation on both Ca9-22 and Cal-27 cells. Consistently, the activities of metastasis-associated metalloproteinases MMP-2 and MMP-9 were attenuated in BubR1 knockdown Ca9-22 cells, suggesting the role of BubR1 in promotion of OSCC migration. Our present study defines an alternative pathway in promoting metastasis of OSCC cells, and the expression of BubR1 could be a prognostic index in OSCC patients. |
format | Online Article Text |
id | pubmed-4519889 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-45198892015-08-03 BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 Chou, Chou-Kit Wu, Chang-Yi Chen, Jeff Yi-Fu Ng, Ming-Chong Wang, Hui-Min David Chen, Jen-Hao Yuan, Shyng-Shiou F. Tsai, Eing-Mei Chang, Jan-Gowth Chiu, Chien-Chih Int J Mol Sci Article BubR1 is a critical component of spindle assembly checkpoint, ensuring proper chromatin segregation during mitosis. Recent studies showed that BubR1 was overexpressed in many cancer cells, including oral squamous cell carcinomas (OSCC). However, the effect of BubR1 on metastasis of OSCC remains unclear. This study aimed to unravel the role of BubR1 in the progression of OSCC and confirm the expression of BubR1 in a panel of malignant OSCC cell lines with different invasive abilities. The results of quantitative real-time PCR showed that the mRNA level of BubR1 was markedly increased in four OSCC cell lines, Ca9-22, HSC3, SCC9 and Cal-27 cells, compared to two normal cells, normal human oral keratinocytes (HOK) and human gingival fibroblasts (HGF). Moreover, the expression of BubR1 in these four OSCC cell lines was positively correlated with their motility. Immunofluorescence revealed that BubR1 was mostly localized in the cytosol of human gingival carcinoma Ca9-22 cells. BubR1 knockdown significantly decreased cellular invasion but slightly affect cellular proliferation on both Ca9-22 and Cal-27 cells. Consistently, the activities of metastasis-associated metalloproteinases MMP-2 and MMP-9 were attenuated in BubR1 knockdown Ca9-22 cells, suggesting the role of BubR1 in promotion of OSCC migration. Our present study defines an alternative pathway in promoting metastasis of OSCC cells, and the expression of BubR1 could be a prognostic index in OSCC patients. MDPI 2015-07-03 /pmc/articles/PMC4519889/ /pubmed/26151845 http://dx.doi.org/10.3390/ijms160715104 Text en © 2015 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Chou, Chou-Kit Wu, Chang-Yi Chen, Jeff Yi-Fu Ng, Ming-Chong Wang, Hui-Min David Chen, Jen-Hao Yuan, Shyng-Shiou F. Tsai, Eing-Mei Chang, Jan-Gowth Chiu, Chien-Chih BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title | BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title_full | BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title_fullStr | BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title_full_unstemmed | BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title_short | BubR1 Acts as a Promoter in Cellular Motility of Human Oral Squamous Cancer Cells through Regulating MMP-2 and MMP-9 |
title_sort | bubr1 acts as a promoter in cellular motility of human oral squamous cancer cells through regulating mmp-2 and mmp-9 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4519889/ https://www.ncbi.nlm.nih.gov/pubmed/26151845 http://dx.doi.org/10.3390/ijms160715104 |
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