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Fig. 5 | Clinical Epigenetics

Fig. 5

From: Combined inhibition of histone deacetylase and cytidine deaminase improves epigenetic potency of decitabine in colorectal adenocarcinomas

Fig. 5

Human chromosomal maps of decitabine and PBA responsive genes. A Chromosomal locations of up- and downregulated genes following decitabine (A1), PBA (A2) and the combined drug treatment (A3). The histograms provide a quantitative account of the number of responsive genes on each chromosome. B Regulation of the lncRNA XIST and its target genes. Based on the lncRNA–mRNA interaction resource starBase v2.0 and LncRRIsearch, we identified NDRG1 and SEMA6A as target of XIST (B1). B2 The gene expression of XIST, NDRG1 and SEMA6A is significantly repressed in COAD tumor samples when compared to histologically proven adjacent normal tissue. The data refer to 275 patients retrieved from the TCGA public repository. B3 NDRG1 and SEMA6A are hyper-methylated in COAD tumor samples when compared to histologically proven adjacent normal tissue (B3). B4 Regulation of XIST, NDRG1 and SEMA6A in Caco-2 cells following drug treatment. XIST gene expression is highly dependent on the combined decitabine/PBA treatment, whereas NDRG1 and SEMA6A responded to single PBA treatment. B5 Kaplan–Meier survival plots for XIST and SEMA6 in low- and high-expression COAD patients. We retrieved the gene expression data of 275 COAD patients from the TCGA public repository, and although not statistically significant, the data imply better survival in high-expression individuals. C Drug-responsive tumor-suppressor genes and anti-apoptosis genes are linked to chromosomal hotspots of COAD patients

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