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Rab25 as a tumour suppressor in colon carcinogenesis

Recent investigations have increasingly focussed attention on the roles of intracellular vesicle trafficking in the regulation of epithelial polarity and transformation. Rab25, an epithelial-specific member of the Rab family of small GTPases, has been associated with several epithelial cancers. Wher...

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Detalles Bibliográficos
Autores principales: Goldenring, J R, Nam, K T
Formato: Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039820/
https://www.ncbi.nlm.nih.gov/pubmed/21063400
http://dx.doi.org/10.1038/sj.bjc.6605983
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author Goldenring, J R
Nam, K T
author_facet Goldenring, J R
Nam, K T
author_sort Goldenring, J R
collection PubMed
description Recent investigations have increasingly focussed attention on the roles of intracellular vesicle trafficking in the regulation of epithelial polarity and transformation. Rab25, an epithelial-specific member of the Rab family of small GTPases, has been associated with several epithelial cancers. Whereas Rab25 overexpression is associated with ovarian cancer aggressive behaviour, Rab25 expression is decreased in human colon cancers independent of stage. Recent studies of mouse models of intestinal and colonic neoplasia have demonstrated that Rab25 deficiency markedly promotes the development of neoplasia. Some of these effects appear related to alterations in β1-integrin trafficking to the cell surface. These findings all suggest that Rab25 is a tumour suppressor for colonic neoplasia.
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spelling pubmed-30398202012-01-04 Rab25 as a tumour suppressor in colon carcinogenesis Goldenring, J R Nam, K T Br J Cancer Minireview Recent investigations have increasingly focussed attention on the roles of intracellular vesicle trafficking in the regulation of epithelial polarity and transformation. Rab25, an epithelial-specific member of the Rab family of small GTPases, has been associated with several epithelial cancers. Whereas Rab25 overexpression is associated with ovarian cancer aggressive behaviour, Rab25 expression is decreased in human colon cancers independent of stage. Recent studies of mouse models of intestinal and colonic neoplasia have demonstrated that Rab25 deficiency markedly promotes the development of neoplasia. Some of these effects appear related to alterations in β1-integrin trafficking to the cell surface. These findings all suggest that Rab25 is a tumour suppressor for colonic neoplasia. Nature Publishing Group 2011-01-04 2010-11-09 /pmc/articles/PMC3039820/ /pubmed/21063400 http://dx.doi.org/10.1038/sj.bjc.6605983 Text en Copyright © 2011 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 Minireview
Goldenring, J R
Nam, K T
Rab25 as a tumour suppressor in colon carcinogenesis
title Rab25 as a tumour suppressor in colon carcinogenesis
title_full Rab25 as a tumour suppressor in colon carcinogenesis
title_fullStr Rab25 as a tumour suppressor in colon carcinogenesis
title_full_unstemmed Rab25 as a tumour suppressor in colon carcinogenesis
title_short Rab25 as a tumour suppressor in colon carcinogenesis
title_sort rab25 as a tumour suppressor in colon carcinogenesis
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3039820/
https://www.ncbi.nlm.nih.gov/pubmed/21063400
http://dx.doi.org/10.1038/sj.bjc.6605983
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