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Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells
BACKGROUND: It is known that aurora B, a chromosomal passenger protein responsible for the proper progression of mitosis and cytokinesis, is overexpressed throughout the cell cycle in cancer cells. Overexpression of aurora B produced multinuclearity and induced aggressive metastasis, suggesting that...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2005
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298314/ https://www.ncbi.nlm.nih.gov/pubmed/16281968 http://dx.doi.org/10.1186/1475-2867-5-31 |
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author | Abdullah, Ash-shafie Foong, Charlene Murata-Hori, Maki |
author_facet | Abdullah, Ash-shafie Foong, Charlene Murata-Hori, Maki |
author_sort | Abdullah, Ash-shafie |
collection | PubMed |
description | BACKGROUND: It is known that aurora B, a chromosomal passenger protein responsible for the proper progression of mitosis and cytokinesis, is overexpressed throughout the cell cycle in cancer cells. Overexpression of aurora B produced multinuclearity and induced aggressive metastasis, suggesting that overexpressed aurora B has multiple functions in cancer development. However, the detailed dynamics and functions of overexpressed aurora B are poorly understood. RESULTS: We overexpressed GFP fused aurora B kinase in normal rat kidney epithelial cells. Using spinning disk confocal microscopy, we found that overexpressed aurora B-GFP was predominantly localized in the nucleus and along the cortex as a dot-like or short filamentous structure during interphase. Time-lapse imaging revealed that a cytoplasmic fraction of overexpressed aurora B-GFP was incorporated into the nucleus after cell division. Immunofluorescence studies showed that the nuclear fraction of overexpressed aurora B did not induce ectopic phosphorylation of histone H3 after cell division. The cytoplasmic fraction of overexpressed aurora B-GFP was mainly associated with cortical actin filaments but not stress fibers. Myosin II regulatory light chain, one of the possible targets for aurora B, did not colocalize with cortical aurora B-GFP, suggesting that overexpressed aurora B did not promote phosphorylation of myosin II regulatory light chain in interphase cells. CONCLUSION: We conclude that overexpressed aurora B has a specific localization pattern in interphase cells. Based on our findings, we propose that overexpressed aurora B targets the nuclear and cortical proteins during interphase, which may contribute to cancer development and tumor metastasis. |
format | Text |
id | pubmed-1298314 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2005 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-12983142006-11-24 Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells Abdullah, Ash-shafie Foong, Charlene Murata-Hori, Maki Cancer Cell Int Primary Research BACKGROUND: It is known that aurora B, a chromosomal passenger protein responsible for the proper progression of mitosis and cytokinesis, is overexpressed throughout the cell cycle in cancer cells. Overexpression of aurora B produced multinuclearity and induced aggressive metastasis, suggesting that overexpressed aurora B has multiple functions in cancer development. However, the detailed dynamics and functions of overexpressed aurora B are poorly understood. RESULTS: We overexpressed GFP fused aurora B kinase in normal rat kidney epithelial cells. Using spinning disk confocal microscopy, we found that overexpressed aurora B-GFP was predominantly localized in the nucleus and along the cortex as a dot-like or short filamentous structure during interphase. Time-lapse imaging revealed that a cytoplasmic fraction of overexpressed aurora B-GFP was incorporated into the nucleus after cell division. Immunofluorescence studies showed that the nuclear fraction of overexpressed aurora B did not induce ectopic phosphorylation of histone H3 after cell division. The cytoplasmic fraction of overexpressed aurora B-GFP was mainly associated with cortical actin filaments but not stress fibers. Myosin II regulatory light chain, one of the possible targets for aurora B, did not colocalize with cortical aurora B-GFP, suggesting that overexpressed aurora B did not promote phosphorylation of myosin II regulatory light chain in interphase cells. CONCLUSION: We conclude that overexpressed aurora B has a specific localization pattern in interphase cells. Based on our findings, we propose that overexpressed aurora B targets the nuclear and cortical proteins during interphase, which may contribute to cancer development and tumor metastasis. BioMed Central 2005-11-09 /pmc/articles/PMC1298314/ /pubmed/16281968 http://dx.doi.org/10.1186/1475-2867-5-31 Text en Copyright © 2005 Abdullah et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Primary Research Abdullah, Ash-shafie Foong, Charlene Murata-Hori, Maki Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title | Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title_full | Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title_fullStr | Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title_full_unstemmed | Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title_short | Specific distribution of overexpressed aurora B kinase in interphase normal epithelial cells |
title_sort | specific distribution of overexpressed aurora b kinase in interphase normal epithelial cells |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1298314/ https://www.ncbi.nlm.nih.gov/pubmed/16281968 http://dx.doi.org/10.1186/1475-2867-5-31 |
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