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Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer
BACKGROUND: UbcH10 participates in proper metaphase to anaphase transition, and abrogation of UbcH10 results in the premature separation of sister chromatids. To assess the potential role of UbcH10 in colon cancer progression, we analyzed the clinicopathological relevance of UbcH10 in colon cancer....
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666760/ https://www.ncbi.nlm.nih.gov/pubmed/19302711 http://dx.doi.org/10.1186/1471-2407-9-87 |
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author | Fujita, Takeo Ikeda, Hirokuni Taira, Naruto Hatoh, Shinji Naito, Minoru Doihara, Hiroyoshi |
author_facet | Fujita, Takeo Ikeda, Hirokuni Taira, Naruto Hatoh, Shinji Naito, Minoru Doihara, Hiroyoshi |
author_sort | Fujita, Takeo |
collection | PubMed |
description | BACKGROUND: UbcH10 participates in proper metaphase to anaphase transition, and abrogation of UbcH10 results in the premature separation of sister chromatids. To assess the potential role of UbcH10 in colon cancer progression, we analyzed the clinicopathological relevance of UbcH10 in colon cancer. METHODS: We firstly screened the expression profile of UbcH10 in various types of cancer tissues as well as cell lines. Thereafter, using the colon cancer cells line, we manipulated the expression of UbcH10 and evaluated the cell cycle profile and cellular proliferations. Furthermore, the clinicopathological significance of UbcH10 was immunohistologically evaluated in patients with colon cancer. Statistical analysis was performed using the student's t-test and Chi-square test. RESULTS: Using the colon cancer cells, depletion of UbcH10 resulted in suppression of cellular growth whereas overexpression of UbcH10 promoted the cellular growth and oncogenic cellular growth. Mitotic population was markedly alternated by the manipulation of UbcH10 expression. Immunohistochemical analysis indicated that UbcH10 was significantly higher in colon cancer tissue compared with normal colon epithelia. Furthermore, the clinicopathological evaluation revealed that UbcH10 was associated with high-grade histological tumors. CONCLUSION: The results show the clinicopathological significance of UbcH10 in the progression of colon cancer. Thus UbcH10 may act as a novel biomarker in patients with colon cancer. |
format | Text |
id | pubmed-2666760 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-26667602009-04-08 Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer Fujita, Takeo Ikeda, Hirokuni Taira, Naruto Hatoh, Shinji Naito, Minoru Doihara, Hiroyoshi BMC Cancer Research Article BACKGROUND: UbcH10 participates in proper metaphase to anaphase transition, and abrogation of UbcH10 results in the premature separation of sister chromatids. To assess the potential role of UbcH10 in colon cancer progression, we analyzed the clinicopathological relevance of UbcH10 in colon cancer. METHODS: We firstly screened the expression profile of UbcH10 in various types of cancer tissues as well as cell lines. Thereafter, using the colon cancer cells line, we manipulated the expression of UbcH10 and evaluated the cell cycle profile and cellular proliferations. Furthermore, the clinicopathological significance of UbcH10 was immunohistologically evaluated in patients with colon cancer. Statistical analysis was performed using the student's t-test and Chi-square test. RESULTS: Using the colon cancer cells, depletion of UbcH10 resulted in suppression of cellular growth whereas overexpression of UbcH10 promoted the cellular growth and oncogenic cellular growth. Mitotic population was markedly alternated by the manipulation of UbcH10 expression. Immunohistochemical analysis indicated that UbcH10 was significantly higher in colon cancer tissue compared with normal colon epithelia. Furthermore, the clinicopathological evaluation revealed that UbcH10 was associated with high-grade histological tumors. CONCLUSION: The results show the clinicopathological significance of UbcH10 in the progression of colon cancer. Thus UbcH10 may act as a novel biomarker in patients with colon cancer. BioMed Central 2009-03-21 /pmc/articles/PMC2666760/ /pubmed/19302711 http://dx.doi.org/10.1186/1471-2407-9-87 Text en Copyright ©2009 Fujita 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 Fujita, Takeo Ikeda, Hirokuni Taira, Naruto Hatoh, Shinji Naito, Minoru Doihara, Hiroyoshi Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title | Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title_full | Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title_fullStr | Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title_full_unstemmed | Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title_short | Overexpression of UbcH10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
title_sort | overexpression of ubch10 alternates the cell cycle profile and accelerate the tumor proliferation in colon cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666760/ https://www.ncbi.nlm.nih.gov/pubmed/19302711 http://dx.doi.org/10.1186/1471-2407-9-87 |
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