MEK5 overexpression is associated with the occurrence and development of colorectal cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12

AUTHORS

Dechang Diao, Lei Wang, Jin Wan, Zhiqiang Chen, Junsheng Peng, Huanliang Liu, Xinlin Chen, Wei Wang, Liaonan Zou

ABSTRACT

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. More... »

PAGES

302

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12885-016-2327-9

DOI

http://dx.doi.org/10.1186/s12885-016-2327-9

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https://app.dimensions.ai/details/publication/pub.1025902266

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27160304


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