1. Cigarette smoke condensate induces differential expression and promoter methylation profiles of critical genes involved in lung cancer in NL-20 lung cells in vitro: short-term and chronic exposure.
- Author
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Word B, Lyn-Cook LE Jr, Mwamba B, Wang H, Lyn-Cook B, and Hammons G
- Subjects
- Apoptosis Regulatory Proteins genetics, Cadherins genetics, Calcium-Calmodulin-Dependent Protein Kinases genetics, Cell Culture Techniques, Cell Line, Tumor, DNA Modification Methylases genetics, DNA Repair Enzymes genetics, Data Interpretation, Statistical, Death-Associated Protein Kinases, Dose-Response Relationship, Drug, Humans, Lung Neoplasms pathology, Polymerase Chain Reaction, Promoter Regions, Genetic, Tumor Suppressor Proteins genetics, Biomarkers, Tumor genetics, DNA Methylation genetics, Gene Expression, Lung Neoplasms etiology, Lung Neoplasms genetics, Smoking adverse effects
- Abstract
Establishing early diagnostic markers of harm is critical for effective prevention programs and regulation of tobacco products. This study examined effects of cigarette smoke condensate (CSC) on expression and promoter methylation profile of critical genes (DAPK, ECAD, MGMT, and RASSF1A) involved in lung cancer development in different human lung cell lines. NL-20 cells were treated with 0.1-100 μg/ml of CSC for 24 to 72 hrs for short-term exposures. DAPK expression or methylation status was not significantly affected. However, CSC treatment resulted in changes in expression and promoter methylation profile of ECAD, MGMT, and RASSF1A. For chronic studies, cells were exposed to 1 or 10 μg/ml CSC up to 28 days. Cells showed morphological changes associated with transformation and changes in invasion capacities and global methylation status. This study provides critical data suggesting that epigenetic changes could serve as an early biomarker of harm due to exposure to cigarette smoke.
- Published
- 2013
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