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. 2016 Feb 2;7(9):9788–9800. doi: 10.18632/oncotarget.7125

Figure 3. CagA-induced DNMT1 upregulation is responsible for MGMT promoter hypermethylation and its expression loss.

Figure 3

(A) Immunohistochemical staining of DNMTs in HP-associated tissues. A marked elevation of DNMT1 is found in CagA+ tissues compared with CagA− tissues, whereas no difference in DNMT3a or DNMT3b expression is observed between groups. (B and C) mRNA and protein expression of DNMTs in HP-associated tissues. Consistent with the results shown in (A), there is a significant difference in DNMT1 expression between CagA+ and CagA− tissues, while DNMT3a or DNMT3b expression remains unchanged in different groups. (D and E) DNMTs expression in CagA+ cells and HP cocultured cells analysed by WB. A remarkable DNMT1 upregulation is found in CagA+ cells and HP cocultured cells compared with control groups while no difference of DNMT3a and DNMT3b exists between groups. (F) Immunocytochemical analysis of DNMT1 expression in CagA+ SGC-7901. A much stronger positive reaction is confirmed in CagA+ cells compared with control groups. (G) MGMT hypermethylation is reversed by DNMT1 inhibition. (UP) DNMT1 and MGMT expression is reversed by siRNA or inhibitor (5-aza-cdr) of DNMT1. (DOWN) MGMT hypermethylation is reversed by DNMT1 siRNA or its inhibitor. The graph represents densitometric analysis of the bands obtained for each signal. Results are expressed as relative expression compared with control cells (*p < 0.05). Each value is the mean ± SD of three experiments.