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Fig. 1 | Journal of Experimental & Clinical Cancer Research

Fig. 1

From: Methylglyoxal: a novel upstream regulator of DNA methylation

Fig. 1

GLO1-depleted MDA-MB-231 breast cancer cells exhibit major DNA hypermethylation and loss of metastasis-related TSGs. A and B Pie charts summarizing the proportion of hypomethylation (FDR < 0.05, Δβ < -0.2) and hypermethylation (FDR < 0.05, Δβ > 0.2) within differentially methylated CpGs (DMCs) found in MDA-MB-231 cells and mouse xenografts, respectively. C Heatmap representing unsupervised clustering of DMCs (rows) identified between control (shNT, n = 3) and GLO1-depleted (shGLO1, n = 6) cells (columns) and their corresponding status in xenograft methylation data. Color key scale blue: low methylation and orange: high methylation. D Proportion of hypo- and hypermethylated DMCs distributed across the genome regulatory regions. Mixed regions correspond to Infinium array probes referring to either promoter or enhancer, according to the considered cell line. E Tumor suppressor gene activated (TSG-A) and oncogene inhibited (OG-I) pathways enriched in genes that were affected by hypermethylation in GLO1-depleted cells as estimated from GSEA tool enrichment scores (with FDR < 0.05). For example, P53 knockdown led to down expression of genes that composed the P53 TSG pathway (‘P53_DN.V1_DN’) whose activation (TSG-A) was affected by high methylation (enrichment score). Please refer to Data S8 for more details on TSG-A and OG-I pathways. F Representative metastasis-related TSGs that were hypermethylated and low expressed under MG stress. Data represent the mean values ± SEM of three independent experiments and were analyzed using a one-way analysis of variance (ANOVA) followed by a Dunnett test (** p < 0.01, *** p < 0.001 and **** p < 0.0001)

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