Figure 1: Genome-wide DNA methylation profiling of endocrine-resistant MCF7 cell models. | Nature Communications

Figure 1: Genome-wide DNA methylation profiling of endocrine-resistant MCF7 cell models.

From: DNA methylation of oestrogen-regulated enhancers defines endocrine sensitivity in breast cancer

Figure 1

(a–c) A colorimetric density plot showing correlation between the HM450 methylation profile of the endocrine-resistant MCF7X (a), TAMR (b) and FASR (c) cells and the parent (endocrine-sensitive) MCF7 cells. The plots show that while the methylation profile of the endocrine-resistant cell lines is strongly correlated with the parent MCF7 cells (MCF7X, r2=0.895; TAMR, r2=0.91; FASR, r2=0.848; Pearson’s coefficient), both the MCF7X and TAMR cells predominantly gain DNA methylation, whereas the FASR cells exhibit both hyper- and hypomethylation events relative to parent MCF7 cells. (d) A Venn diagram showing the overlap of HM450 methylation probes that are more heavily methylated in multiple endocrine-resistant cells compared with the parent MCF7 cells (FDR<0.01). (e) A bar plot showing the association of differentially methylated HM450 probes that were common to all endocrine-resistant cell lines (compared with the parent MCF7 cells) across functional/regulatory regions of the genome as determined by MCF7 ChromHMM annotation13. The height of the bars represents the level of enrichment measured as a ratio between the frequency of hypermethylated (dark blue) or hypomethylated (light blue) probes overlapping a functional element over the expected frequency if such overlaps were to occur at random in the genome. Statistically significant enrichments (P value<<0.0001; hypergeometric test) are marked with an asterisk. The numbers of commonly hyper/hypomethylated probes located within each specific region are presented in the respective column.

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