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BMC Cancer

, 12:191

First Online: 28 May 2012Received: 25 October 2011Accepted: 14 May 2012DOI: 10.1186-1471-2407-12-191

Cite this article as: Nakamura, K., Kodama, J., Hongo, A. et al. BMC Cancer 2012 12: 191. doi:10.1186-1471-2407-12-191

Abstract

BackgroundExtracellular matrix metalloproteinase inducer Emmprin-CD147 is a transmembrane glycoprotein that belongs to the immunoglobulin superfamily. Enriched on the surface of many tumor cells, emmprin promotes tumor growth, invasion, metastasis and angiogenesis. We evaluated the clinical importance of emmprin and investigated its role in endometrial cancer.

MethodsEmmprin expression was examined in uterine normal endometrium, endometrial hyperplasia and cancer specimens by immunohistochemistry. In addition, the biological functions and inhibitory effects of an emmprin knockdown were investigated in HEC-50B and KLE endometrial cancer cell lines.

ResultsThe levels of emmprin expression were significantly increased in the endometrial cancer specimens compared with the normal endometrium and endometrial hyperplasia specimens p < 0.05. The disease-free survival DFS and overall survival OS rates of patients with high emmprin expression were significantly higher than those of patients with low emmprin expression DFS: p < 0.001; OS: p < 0.001. Emmprin knockdown by the siRNA led to cell proliferation, migration and invasion through TGF-β, EGF, NF-κB, VEGF, MMP-2, and MMP-9 expression, which in turn resulted in increased levels of E-cadherin and reduced levels of Vimentin and Snail in endometrial cancer.

ConclusionsThe present findings suggest that low emmprin expression might be a predictor of favorable prognosis in endometrial cancer patients, and that emmprin may represent a potential therapeutic target for endometrial cancer.

KeywordsEndometrial cancer Emmprin Epithelial-mesenchymal transition Predictor of favorable prognosis Potential therapeutic target AbbreviationsEmmprinExtracellular matrix metalloproteinase inducer

ECMExtracellular matrix

NF-κBNuclear factor kappa B

JNKc-Jun N-terminal kinase

VEGFVascular endothelial cell growth factor

EMTEpithelial-mesenchymal transition

TGFTransforming growth factor

IGFInsulin-like growth factor

EGFEpidermal growth factor

TNFTumor necrosis factor

SIP1Smadinteracting protein 1

FIGOInternational Federation of Gynecology and Obstetrics

DFSDisease-free survival

OSOverall survival

DMEMDulbecco’s modified eagle’s medium

FBSFetal bovine serum

GAPDHGlyceraldehyde- 3-phosphate dehydrogenase

ERKExtracellular signal-regulated kinase.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2407-12-191 contains supplementary material, which is available to authorized users.

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Autor: Keiichiro Nakamura - Junichi Kodama - Atsushi Hongo - Yuji Hiramatsu

Fuente: https://link.springer.com/







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