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MEK5 overexpression is associated with the occurrence and development of colorectal cancer
BACKGROUND: Mitogen/extracellular signal-regulated kinase kinase-5 (MEK5) has been confirmed to play a pivotal role in tumor carcinogenesis and progression. However, few studies have investigated the role of MEK5 in colorectal cancer (CRC). METHODS: MEK5 expression was determined by immunohistochemi...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4862041/ https://www.ncbi.nlm.nih.gov/pubmed/27160304 http://dx.doi.org/10.1186/s12885-016-2327-9 |
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author | Diao, Dechang Wang, Lei Wan, Jin Chen, Zhiqiang Peng, Junsheng Liu, Huanliang Chen, Xinlin Wang, Wei Zou, Liaonan |
author_facet | Diao, Dechang Wang, Lei Wan, Jin Chen, Zhiqiang Peng, Junsheng Liu, Huanliang Chen, Xinlin Wang, Wei Zou, Liaonan |
author_sort | Diao, Dechang |
collection | PubMed |
description | BACKGROUND: Mitogen/extracellular signal-regulated kinase kinase-5 (MEK5) has been confirmed to play a pivotal role in tumor carcinogenesis and progression. However, few studies have investigated the role of MEK5 in colorectal cancer (CRC). METHODS: MEK5 expression was determined by immunohistochemistry (IHC) in tissue microarrays (TMAs) containing 2 groups of tissues, and western blotting was used to confirm MEK5 expression in 8 cases of primary CRC tissues and paired normal mucosa. RNA interference was used to verify the biological function of MEK5 gene in the development of CRC. RESULTS: IHC revealed the expression of MEK5 was higher in tumor tissues (38.1 %), compared with adjacent normal tissue (8.3 %). Western blot showed that, MEK5 expression was upregulated in CRC tumor tissues compared with normal tissue. Analysis of clinical pathology parameters indicated MEK5 overexpression was significantly correlated with the depth of invasion, lymph node metastasis, distant metastasis and histological grade. Survival analysis revealed that MEK5 overexpression negatively correlated with cancer-free survival (hazard ratio 1.64, P = 0.017). RNA interference-mediated knockdown of MEK5 in SW480 colon cancer cells decreased their proliferation, division, migration and invasiveness in vitro and slowed down tumors growth in mice engrafted with the cells. CONCLUSION: MEK5 plays an important role in CRC progression and may be a potential molecular target for the treatment of CRC. |
format | Online Article Text |
id | pubmed-4862041 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-48620412016-05-11 MEK5 overexpression is associated with the occurrence and development of colorectal cancer Diao, Dechang Wang, Lei Wan, Jin Chen, Zhiqiang Peng, Junsheng Liu, Huanliang Chen, Xinlin Wang, Wei Zou, Liaonan BMC Cancer Research Article BACKGROUND: Mitogen/extracellular signal-regulated kinase kinase-5 (MEK5) has been confirmed to play a pivotal role in tumor carcinogenesis and progression. However, few studies have investigated the role of MEK5 in colorectal cancer (CRC). METHODS: MEK5 expression was determined by immunohistochemistry (IHC) in tissue microarrays (TMAs) containing 2 groups of tissues, and western blotting was used to confirm MEK5 expression in 8 cases of primary CRC tissues and paired normal mucosa. RNA interference was used to verify the biological function of MEK5 gene in the development of CRC. RESULTS: IHC revealed the expression of MEK5 was higher in tumor tissues (38.1 %), compared with adjacent normal tissue (8.3 %). Western blot showed that, MEK5 expression was upregulated in CRC tumor tissues compared with normal tissue. Analysis of clinical pathology parameters indicated MEK5 overexpression was significantly correlated with the depth of invasion, lymph node metastasis, distant metastasis and histological grade. Survival analysis revealed that MEK5 overexpression negatively correlated with cancer-free survival (hazard ratio 1.64, P = 0.017). RNA interference-mediated knockdown of MEK5 in SW480 colon cancer cells decreased their proliferation, division, migration and invasiveness in vitro and slowed down tumors growth in mice engrafted with the cells. CONCLUSION: MEK5 plays an important role in CRC progression and may be a potential molecular target for the treatment of CRC. BioMed Central 2016-05-09 /pmc/articles/PMC4862041/ /pubmed/27160304 http://dx.doi.org/10.1186/s12885-016-2327-9 Text en © Diao et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Diao, Dechang Wang, Lei Wan, Jin Chen, Zhiqiang Peng, Junsheng Liu, Huanliang Chen, Xinlin Wang, Wei Zou, Liaonan MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title | MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title_full | MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title_fullStr | MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title_full_unstemmed | MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title_short | MEK5 overexpression is associated with the occurrence and development of colorectal cancer |
title_sort | mek5 overexpression is associated with the occurrence and development of colorectal cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4862041/ https://www.ncbi.nlm.nih.gov/pubmed/27160304 http://dx.doi.org/10.1186/s12885-016-2327-9 |
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