Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-5-11
pubmed:databankReference
pubmed:abstractText
Cigarette smoking is the main risk factor for the development of squamous cell lung carcinoma (SCC). However, the smoking-related molecular changes in SCC have not been studied. Gene expression studies in both histologically normal bronchial epithelium and SCC epithelial samples identified genes differentially expressed between current and ex-smokers. Subsequently, expression levels of the smoking-related genes in normal bronchial epithelium were compared with those in SCC cells, since we hypothesized that the smoking-induced changes would be also deregulated in SCC. Gene expression profiles were generated using Agilent whole human genome microarrays on laser-microdissected normal bronchial epithelium and SCC samples. Expression levels of 246 genes, mainly related to oxidative stress response, were significantly different between normal bronchial epithelium of current and ex-smokers. Such a differential gene expression profile did not exist in SCC cells of smokers and ex-smokers. Interestingly, when comparing SCC and normal bronchial epithelium from ex-smokers, the vast majority of these 246 genes were also deregulated in SCC. When comparing SCC with normal epithelium from smokers, 22% of the up-regulated genes showed a similar high expression in SCC whereas 79% of the down-regulated genes were even further reduced in SCC as compared to current smokers. The down-regulated genes included several tumour suppressor genes, such as C9orf9, INHBB, LRIG1, SCGB3A1, SERPINI2, STEAP3 and ZMYND10. Thus, our study shows that the majority of genes up-regulated in normal bronchial epithelium of current smokers show similar high expression levels in SCC, while down-regulated genes are even further repressed in SCC. Our data indicate that smoking-related changes in normal bronchial epithelial cells persist in malignant transformed squamous cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1096-9896
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
218
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
182-91
pubmed:meshHeading
pubmed-meshheading:19334046-Aged, pubmed-meshheading:19334046-Bronchi, pubmed-meshheading:19334046-Carcinoma, Squamous Cell, pubmed-meshheading:19334046-Case-Control Studies, pubmed-meshheading:19334046-Female, pubmed-meshheading:19334046-Gene Expression Profiling, pubmed-meshheading:19334046-Gene Expression Regulation, Neoplastic, pubmed-meshheading:19334046-Humans, pubmed-meshheading:19334046-Immunohistochemistry, pubmed-meshheading:19334046-Lung Neoplasms, pubmed-meshheading:19334046-Male, pubmed-meshheading:19334046-Middle Aged, pubmed-meshheading:19334046-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:19334046-Respiratory Mucosa, pubmed-meshheading:19334046-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:19334046-Smoking, pubmed-meshheading:19334046-Smoking Cessation
pubmed:year
2009
pubmed:articleTitle
Current smoking-specific gene expression signature in normal bronchial epithelium is enhanced in squamous cell lung cancer.
pubmed:affiliation
Department of Pathology, University Medical Centre Groningen, Groningen, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't