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MEK5 overexpression is associated with the occurrence and development of colorectal cancer.

Authors :
Dechang Diao
Lei Wang
Jin Wan
Zhiqiang Chen
Junsheng Peng
Huanliang Liu
Xinlin Chen
Wei Wang
Liaonan Zou
Diao, Dechang
Wang, Lei
Wan, Jin
Chen, Zhiqiang
Peng, Junsheng
Liu, Huanliang
Chen, Xinlin
Wang, Wei
Zou, Liaonan
Source :
BMC Cancer; 5/9/2016, Vol. 16, p1-12, 12p, 1 Color Photograph, 1 Diagram, 4 Charts, 4 Graphs
Publication Year :
2016

Abstract

<bold>Background: </bold>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).<bold>Methods: </bold>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.<bold>Results: </bold>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, Pā€‰=ā€‰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.<bold>Conclusion: </bold>MEK5 plays an important role in CRC progression and may be a potential molecular target for the treatment of CRC. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
14712407
Volume :
16
Database :
Complementary Index
Journal :
BMC Cancer
Publication Type :
Academic Journal
Accession number :
115259316
Full Text :
https://doi.org/10.1186/s12885-016-2327-9