Document Detail


ENO1, a potential prognostic head and neck cancer marker, promotes transformation partly via chemokine CCL20 induction.
MedLine Citation:
PMID:  20435467     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The success of using glycolytic inhibitors for cancer treatment depends on studying the individual role of frequently deregulated glycolytic genes in cancer. This report aims to study the prognostic implication, and determine the cellular role and action mechanism of glycolytic ENO1 overexpression in head and neck cancer. The relationship of ENO1 mRNA expression in 44-pair clinical specimens with patient clinicopathologic characteristics was analysed by semi-quantitative RT-PCR, Kaplan-Meier survival curve and Cox model analyses. Following ectopic ENO1 expression or knockdown, we studied the proliferative, migratory, invasive, colony-forming and tumourigenic abilities of ENO1-genetically altered cells. DNA microarray analysis was used to identify downstream targets responsible for the ENO1 action in the cells. The expression of ENO1 mRNA was increased in 68% of tumour (T) specimens when compared to their normal (N) counterparts, and positively associated with clinical progression (p<0.05). High ENO1 expression (T/N2) was frequently observed in the patients with large primary tumours, late clinical stages or advanced neck metastasis. Moreover, high ENO1 patients had significantly poorer clinical outcomes than low expressers (T/N<2). Ectopic ENO1 expression stimulated cell transformation, invasion and tongue tumour formation. ENO1 knockdown abrogated the stimulation. Suppression of ENO1-induced proinflammatory CCL20 chemokine expression significantly attenuated its stimulatory effects on cell transformation and invasion. A concordant expression of ENO1 and CCL20 was validated both in ENO1-expressing cells and in clinical specimens. Together, we demonstrate a prognostic role of ENO1 overexpression in head and neck cancer and ENO1-mediated promotion of cell transformation and invasion partly via induced CCL20 expression.
Authors:
Sen-Tien Tsai; I-Hsiu Chien; Wen-Hao Shen; Yi-Zih Kuo; Ying-Tai Jin; Tung-Yiu Wong; Jenn-Ren Hsiao; Hsing-Ping Wang; Neng-Yao Shih; Li-Wha Wu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of cancer (Oxford, England : 1990)     Volume:  46     ISSN:  1879-0852     ISO Abbreviation:  Eur. J. Cancer     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-06-10     Completed Date:  2010-10-06     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9005373     Medline TA:  Eur J Cancer     Country:  England    
Other Details:
Languages:  eng     Pagination:  1712-23     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Ltd. All rights reserved.
Affiliation:
Department of Otolaryngology, National Cheng Kung University Hospital, Tainan 70428, Taiwan, ROC.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Transformation, Neoplastic / genetics,  metabolism*
Chemokine CCL20 / metabolism*
DNA-Binding Proteins / genetics,  metabolism,  physiology*
Female
Gene Expression
Gene Knockdown Techniques
Humans
Male
Mice
Mice, Nude
Middle Aged
Mouth Neoplasms / enzymology*,  genetics,  pathology
Neoplasm Invasiveness
Phosphopyruvate Hydratase / genetics,  metabolism,  physiology*
Prognosis
RNA, Messenger / metabolism
RNA, Neoplasm / metabolism
Reverse Transcriptase Polymerase Chain Reaction
Tongue Neoplasms / enzymology,  pathology
Tumor Cells, Cultured
Tumor Markers, Biological / genetics,  metabolism,  physiology*
Tumor Suppressor Proteins / genetics,  metabolism,  physiology*
Up-Regulation
Chemical
Reg. No./Substance:
0/Chemokine CCL20; 0/DNA-Binding Proteins; 0/RNA, Messenger; 0/RNA, Neoplasm; 0/Tumor Markers, Biological; 0/Tumor Suppressor Proteins; EC 4.2.1.11/ENO1 protein, human; EC 4.2.1.11/Phosphopyruvate Hydratase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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