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Comparison of gene expression levels for ADAR, ADARB1, and ADARB2 in smokers and non-smokers, indicating RNA editing modulation.
Tobacco exposure is commonly linked to airway epithelium and lung diseases, yet its impact on the enzymes that catalyze adenosine-to-inosine (A-to-I) RNA editing remains unclear. The goal of this research is to compare the three gene expression levels, ADAR, ADARB1, ADARB2, between smokers and non-smoker, which play an important role in RNA editing and cellular regulation. RNA-sequence count data for smokers (362 samples) and non-smokers (635) were obtained from the GEO publication “Cigarette Smoking-Associated Isoform Switching and 3’ UTR Lengthening Via Alternative Polyadenylation” (GSE171730). Data obtained was first applied with log₂-transformation to dampen outliers, then compared with T-test. The result of the study shows that smoking had no significant effect on ADAR1, but produced robust up-regulation of ADARB1 and ADARB2. These results indicate that tobacco selectively enhances expression of two ADAR paralogs while sparing the ubiquitously expressed ADAR1, pointing to a targeted modulation of the RNA-editing machinery in smokers. Such selective induction may shift global A-to-I editing profiles and contribute to smoking-associated disease risk.
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Jing-Quan Shi (2025) studied this question.
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