Fig. 4: CBX7 is inactivated by promoter hypermethylation mediated by DNMT1 and DNMT3A in UBC. | Cell Death & Disease

Fig. 4: CBX7 is inactivated by promoter hypermethylation mediated by DNMT1 and DNMT3A in UBC.

From: CBX7 suppresses urinary bladder cancer progression via modulating AKR1B10–ERK signaling

Fig. 4: CBX7 is inactivated by promoter hypermethylation mediated by DNMT1 and DNMT3A in UBC.

a Pearson correlation analysis showed a significant negative correlation between CBX7 methylation level and mRNA expression from TCGA dataset. b Kaplan–Meier survival plot was constructed according to the methylation level. c, d mRNA and protein levels of CBX7 were restored in UBC cells after treatment with 5-Aza-CdR at 10 μM for the indicated times. e, f Bisulfite genomic sequencing (BGS) analysis of CBX7 CpG island region. Methylation status of CBX7 was observed in UBC cell lines and paired UBC tissues (T) and their adjacent noncancerous tissues (N). g CBX7 mRNA levels were examined in DNMT1, DNMT3A, or DNMT3B-silenced 5637 and UMUC-3 cells by qRT-PCR. h, i Western blotting results showed that knockdown of DNMT1 and DNMT3A in 5637 and UMUC-3 cells significantly elevated the level of CBX7. Data are presented as means ± SD from three independent replicates. *p < 0.05, **p < 0.01, ***p < 0.001, ns nonsignificant.

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