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. 2016 May 19;7(31):49107–49121. doi: 10.18632/oncotarget.9470

Figure 3. Analysis of CYP1A1 methylation in enhancer regions B (XRE-983) and C (XRE-895), and effect of smoking on methylation levels.

Figure 3

DNA of clinical specimens underwent bisulfite modification followed by methylation-specific PCR (MSP) analyses. (A) Representative gel results of MSP-B (top gel) and unmethylation-specific PCR (USP)-B (bottom gel) of CYP1A1 enhancer in benign prostate hyperplasia (BPH) and prostate cancer (PC) samples. Bar graph: The prevalence of CYP1A1 methylation was significantly lower in prostate cancer (n = 176) than BPH (n = 69) samples as measured by densitometry of gel bands. ***P < 0.001. (B) Representative gel results of MSP-C (top gel) and USP-C (bottom gel) of CYP1A1 enhancer in BPH and prostate cancer (PC) samples. Bar graph: A significant reduction in CYP1A1 methylation levels in prostate cancer (PC) samples were also observed for this site. ***P < 0.001. (C) CYP1A1 methylation levels in relation to tobacco smoker status at all 3 regions. Smoking habit affected the methylation level of CYP1A1 region A. Non-smokers n = 108, Smokers n = 45; *P < 0.05.