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HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells
HuR, a ubiquitously expressed member of the Hu protein family that binds and stabilizes an AU-rich element (ARE)-containing mRNAs, is known to shuttle between the nucleus and the cytoplasm via several export pathways. When normal cells were treated with heat shock, HuR was exported to the cytoplasm...
Autores principales: | , , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2009
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714239/ https://www.ncbi.nlm.nih.gov/pubmed/19513080 http://dx.doi.org/10.1038/sj.bjc.6605084 |
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author | Hasegawa, H Kakuguchi, W Kuroshima, T Kitamura, T Tanaka, S Kitagawa, Y Totsuka, Y Shindoh, M Higashino, F |
author_facet | Hasegawa, H Kakuguchi, W Kuroshima, T Kitamura, T Tanaka, S Kitagawa, Y Totsuka, Y Shindoh, M Higashino, F |
author_sort | Hasegawa, H |
collection | PubMed |
description | HuR, a ubiquitously expressed member of the Hu protein family that binds and stabilizes an AU-rich element (ARE)-containing mRNAs, is known to shuttle between the nucleus and the cytoplasm via several export pathways. When normal cells were treated with heat shock, HuR was exported to the cytoplasm in a chromosome maintenance region 1 (CRM1)-dependent manner. However, in this study, we demonstrate that HuR is exported to the cytoplasm in oral cancer cells even if the cells were treated with the inhibitor of the CRM1-independent export pathway. Immunohistochemical and biochemical analyses showed that HuR existed in both the cytoplasm and the nucleus in oral cancer cells, such as HSC-3 and Ca9.22, but existed entirely inside the nucleus in normal cells. AU-rich element-mRNAs were also exported to the cytoplasm and stabilised in the oral cancer cells, which were inhibited by HuR knockdown. This export of HuR was not affected by at least 7 h of treatment of leptomycin B (LMB), which is an inhibitor of the CRM1-dependent export pathway. These findings suggest that HuR is exported to the cytoplasm in oral carcinoma cells in a different manner from that of normal cells, and is likely to occur through the perturbation of a normal export pathway. |
format | Text |
id | pubmed-2714239 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-27142392010-06-16 HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells Hasegawa, H Kakuguchi, W Kuroshima, T Kitamura, T Tanaka, S Kitagawa, Y Totsuka, Y Shindoh, M Higashino, F Br J Cancer Molecular Diagnostics HuR, a ubiquitously expressed member of the Hu protein family that binds and stabilizes an AU-rich element (ARE)-containing mRNAs, is known to shuttle between the nucleus and the cytoplasm via several export pathways. When normal cells were treated with heat shock, HuR was exported to the cytoplasm in a chromosome maintenance region 1 (CRM1)-dependent manner. However, in this study, we demonstrate that HuR is exported to the cytoplasm in oral cancer cells even if the cells were treated with the inhibitor of the CRM1-independent export pathway. Immunohistochemical and biochemical analyses showed that HuR existed in both the cytoplasm and the nucleus in oral cancer cells, such as HSC-3 and Ca9.22, but existed entirely inside the nucleus in normal cells. AU-rich element-mRNAs were also exported to the cytoplasm and stabilised in the oral cancer cells, which were inhibited by HuR knockdown. This export of HuR was not affected by at least 7 h of treatment of leptomycin B (LMB), which is an inhibitor of the CRM1-dependent export pathway. These findings suggest that HuR is exported to the cytoplasm in oral carcinoma cells in a different manner from that of normal cells, and is likely to occur through the perturbation of a normal export pathway. Nature Publishing Group 2009-06-16 2009-06-09 /pmc/articles/PMC2714239/ /pubmed/19513080 http://dx.doi.org/10.1038/sj.bjc.6605084 Text en Copyright © 2009 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Molecular Diagnostics Hasegawa, H Kakuguchi, W Kuroshima, T Kitamura, T Tanaka, S Kitagawa, Y Totsuka, Y Shindoh, M Higashino, F HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title | HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title_full | HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title_fullStr | HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title_full_unstemmed | HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title_short | HuR is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
title_sort | hur is exported to the cytoplasm in oral cancer cells in a different manner from that of normal cells |
topic | Molecular Diagnostics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2714239/ https://www.ncbi.nlm.nih.gov/pubmed/19513080 http://dx.doi.org/10.1038/sj.bjc.6605084 |
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