Fig. 2

CpG hypermethylation is responsible for the silencing of miR-141 and miR-200c. a Expression of miR-141 and miR-200c in 10 paired PDAC and their surrounding non-cancerous tissues. The mRNA expression was measured by qRT–PCR. U6 was used as internal reference. b Correlation between the expression of miRNA-141 and its CpG methylation level in 37 PDAC tissues using Spearman’s correlation analysis. c Correlation between the expression of miRNA-200c and its CpG methylation level in 37 PDAC tissues using Spearman’s correlation analysis. d Levels of methylation of miR-141 and miR-200c promoter region in human pancreatic ductal epithelial cells (HPDE) and pancreatic cancer cell lines (PANC-1, BxPC-3, HPAF-II, and SW1990). Note the levels of methylation in the pancreatic cell lines were all dramatically higher than HPDE cells. The data were derived from three sets of experiments. Error bars are represented as the mean +/− SD. e Change of methylation levels of miR-141 and miR-200c promoter in pancreatic cancer cell lines in response to 5-Aza-dC treatment. f Relative levels of miR-141 and miR-200c expression in response to 5-Aza-dC treatment in the pancreatic cancer cell lines. For both (e) and (f), Data were derived from three sets of experiments. Error bars are repreented as the mean +/− SD. ^* P < 0.05. Control, cells were left untreated; 5-Aza-dC, cells were treated with 5-Aza-dC