Chest
Original ResearchLung CancerSmoking-Induced Upregulation of AKR1B10 Expression in the Airway Epithelium of Healthy Individuals
Section snippets
Study Population
All subjects were recruited through advertisements in local newspapers, on electronic bulletin boards, and through an ongoing program of free spirometry screening. The evaluation of all individuals was performed at the Department of Genetic Medicine Clinical Research Facility under the auspices of the Weill Cornell National Institutes of Health Clinical Translational Science Center (New York, NY), using Institutional Review Board-approved clinical protocols. Nonsmokers and smokers were
Study Population
A total of 52 large airway samples from 21 healthy nonsmokers and 31 healthy smokers and 109 small airway samples from 51 healthy nonsmokers and 58 healthy smokers were analyzed on Affymetrix HG-U133 Plus 2.0 microarrays (Table 1). For the large airway samples, there were no differences between groups with regard to ancestral background (P > .4), sex (P > .1), and age (P > .2). For the small airway samples, there also were no differences between groups with regard to ancestral background (P >
Discussion
AKR1B10, a member of the AKR family, has been suggested as an early detection marker and treatment target for NSCLC.12 Using microarray analysis to compare gene expression of the airway epithelium in healthy smokers and healthy nonsmokers, we found AKR1B10 was highly upregulated in both large and small airway epithelia of healthy smokers. The microarray data were confirmed at both the mRNA level (TaqMan real-time PCR) and the protein level (Western blot analysis and immunohistochemistry).
Acknowledgments
Author Contributions: Dr R. Wang: contributed to the background research, experimental design, execution and data analysis, TaqMan real-time PCR, in vitro MTT assay, and writing the manuscript.
Dr G. Wang: performed experimental work, including Western analysis.
Ms Ricard: contributed to the retinoic acid experiments.
Ms Ferris: performed experimental work related to immunohistochemistry.
Ms Strulovici-Barel: contributed to compilation and analysis of microarray data.
Ms Salit: contributed to
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Funding/Support: This study was supported, in part, by the National Institutes of Health [R01 HL074326, P50 HL084936, UL1-RR024996, T32 HL094284] and the National Cancer Institute [R01CA097543].
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