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. Author manuscript; available in PMC: 2018 Oct 1.
Published in final edited form as: Cancer Prev Res (Phila). 2017 Aug 29;10(10):588–597. doi: 10.1158/1940-6207.CAPR-17-0198

Figure 3. Tobacco-specific carcinogens induce methylation, DNA adducts, DNA damage and activation of DNMT1.

Figure 3

A) Heat map of metabolites from J82 cells that were treated with NNK (100 μM), BaP (10 μM), with NNK followed by AZA (5μM) (NNK +AZA) and BaP + AZA (FDR<0.25). B) DNA adducts in untreated and treated cells with NNK, BaP, NNK +AZA and BaP + AZA were measured by LC-MS/MS (p-value <0.005). C) Confocal microscopy and quantification analysis of γ-H2AX (green) in J82 cells treated with NNK, NNK+AZA, BaP and BaP+AZA (p<0.0001). D) Western blots and quantification of γ-H2AX protein levels in J82 cells treated with aphidicolin, NNK, and AZA (p<0.0001). β-actin was used as the loading control. Comparison of DNMT1 protein (E) and mRNA (F) expression in tissues of smokers (n=15) and non-smokers (n=15) and their quantification (p<0.05). G) Immunohistochemical analysis of DNMT1 expression in BLCA tissues from smoker and non-smoker.