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Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells
BACKGROUND: ID proteins are dominant negative inhibitors of basic helix-loop-helix transcription factors that have multiple functions during development and cellular differentiation. Ectopic (over-)expression of ID1 extends the lifespan of primary human epithelial cells. High expression levels of ID...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818612/ https://www.ncbi.nlm.nih.gov/pubmed/20070914 http://dx.doi.org/10.1186/1471-2121-11-2 |
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author | Manthey, Carolin Mern, Demissew S Gutmann, Anja Zielinski, Anne J Herz, Corinna Lassmann, Silke Hasskarl, Jens |
author_facet | Manthey, Carolin Mern, Demissew S Gutmann, Anja Zielinski, Anne J Herz, Corinna Lassmann, Silke Hasskarl, Jens |
author_sort | Manthey, Carolin |
collection | PubMed |
description | BACKGROUND: ID proteins are dominant negative inhibitors of basic helix-loop-helix transcription factors that have multiple functions during development and cellular differentiation. Ectopic (over-)expression of ID1 extends the lifespan of primary human epithelial cells. High expression levels of ID1 have been detected in multiple human malignancies, and in some have been correlated with unfavorable clinical prognosis. ID1 protein is localized at the centrosomes and forced (over-)expression of ID1 results in errors during centrosome duplication. RESULTS: Here we analyzed the steady state expression levels of the four ID-proteins in 18 tumor cell lines and assessed the number of centrosome abnormalities. While expression of ID1, ID2, and ID3 was detected, we failed to detect protein expression of ID4. Expression of ID1 correlated with increased supernumerary centrosomes in most cell lines analyzed. CONCLUSIONS: This is the first report that shows that not only ectopic expression in tissue culture but endogenous levels of ID1 modulate centrosome numbers. Thus, our findings support the hypothesis that ID1 interferes with centrosome homeostasis, most likely contributing to genomic instability and associated tumor aggressiveness. |
format | Text |
id | pubmed-2818612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28186122010-02-10 Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells Manthey, Carolin Mern, Demissew S Gutmann, Anja Zielinski, Anne J Herz, Corinna Lassmann, Silke Hasskarl, Jens BMC Cell Biol Research article BACKGROUND: ID proteins are dominant negative inhibitors of basic helix-loop-helix transcription factors that have multiple functions during development and cellular differentiation. Ectopic (over-)expression of ID1 extends the lifespan of primary human epithelial cells. High expression levels of ID1 have been detected in multiple human malignancies, and in some have been correlated with unfavorable clinical prognosis. ID1 protein is localized at the centrosomes and forced (over-)expression of ID1 results in errors during centrosome duplication. RESULTS: Here we analyzed the steady state expression levels of the four ID-proteins in 18 tumor cell lines and assessed the number of centrosome abnormalities. While expression of ID1, ID2, and ID3 was detected, we failed to detect protein expression of ID4. Expression of ID1 correlated with increased supernumerary centrosomes in most cell lines analyzed. CONCLUSIONS: This is the first report that shows that not only ectopic expression in tissue culture but endogenous levels of ID1 modulate centrosome numbers. Thus, our findings support the hypothesis that ID1 interferes with centrosome homeostasis, most likely contributing to genomic instability and associated tumor aggressiveness. BioMed Central 2010-01-14 /pmc/articles/PMC2818612/ /pubmed/20070914 http://dx.doi.org/10.1186/1471-2121-11-2 Text en Copyright ©2010 Manthey 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 | Research article Manthey, Carolin Mern, Demissew S Gutmann, Anja Zielinski, Anne J Herz, Corinna Lassmann, Silke Hasskarl, Jens Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title | Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title_full | Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title_fullStr | Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title_full_unstemmed | Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title_short | Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells |
title_sort | elevated endogenous expression of the dominant negative basic helix-loop-helix protein id1 correlates with significant centrosome abnormalities in human tumor cells |
topic | Research article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2818612/ https://www.ncbi.nlm.nih.gov/pubmed/20070914 http://dx.doi.org/10.1186/1471-2121-11-2 |
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