Linked Life Data

20435467

Source:http://linkedlifedata.com/resource/pubmed/id/20435467

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-6-10
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1879-0852
pubmed:author
pubmed:copyrightInfo
Copyright 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1712-23
pubmed:meshHeading
pubmed-meshheading:20435467-Animals, pubmed-meshheading:20435467-Cell Transformation, Neoplastic, pubmed-meshheading:20435467-Chemokine CCL20, pubmed-meshheading:20435467-DNA-Binding Proteins, pubmed-meshheading:20435467-Female, pubmed-meshheading:20435467-Gene Expression, pubmed-meshheading:20435467-Gene Knockdown Techniques, pubmed-meshheading:20435467-Humans, pubmed-meshheading:20435467-Male, pubmed-meshheading:20435467-Mice, pubmed-meshheading:20435467-Mice, Nude, pubmed-meshheading:20435467-Middle Aged, pubmed-meshheading:20435467-Mouth Neoplasms, pubmed-meshheading:20435467-Neoplasm Invasiveness, pubmed-meshheading:20435467-Phosphopyruvate Hydratase, pubmed-meshheading:20435467-Prognosis, pubmed-meshheading:20435467-RNA, Messenger, pubmed-meshheading:20435467-RNA, Neoplasm, pubmed-meshheading:20435467-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:20435467-Tongue Neoplasms, pubmed-meshheading:20435467-Tumor Cells, Cultured, pubmed-meshheading:20435467-Tumor Markers, Biological, pubmed-meshheading:20435467-Tumor Suppressor Proteins, pubmed-meshheading:20435467-Up-Regulation
pubmed:year
2010
pubmed:articleTitle
ENO1, a potential prognostic head and neck cancer marker, promotes transformation partly via chemokine CCL20 induction.
pubmed:affiliation
Department of Otolaryngology, National Cheng Kung University Hospital, Tainan 70428, Taiwan, ROC.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't