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Fig. 5 | Genome Medicine

Fig. 5

From: Integrative epigenomic and high-throughput functional enhancer profiling reveals determinants of enhancer heterogeneity in gastric cancer

Fig. 5

Cis-analysis of differential enhancers. a Distribution of enhancers associated with copy number. CN-abnormal enhancers represent differential enhancers with altered DNA copy numbers in OCUM1 or SNU16. CN-associated enhancers represent differential enhancers showing concordant changes in H3K27ac signals and DNA copy number. MYC, WDR11, FGFR2, CD44, PDHX, and ING1-associated enhancers are highlighted as they show a statistically significant correlation between enhancer copy numbers with target gene expression levels. b Correlation of H3K27ac signals and ING1 gene expression with the DNA copy numbers for the ING1 enhancer among multiple GC lines. c H3K27ac ChIP-seq and CapSTARR-seq tracks at the enhancer region harboring the ARL4C-associated SNP rs1464264 in OCUM1 and SNU16 cells. d H3K27ac ChIP-seq tracks in GC lines and pcHi-C associations in gastric tissues. The SNP rs1464264 genotype is annotated above the H3K27ac ChIP-seq track in each cell line. Significant chromatin interactions are shown below the axis (green loop). e Differences in expression of ARL4C in three groups of cell lines with different SNP rs1464264 genotypes (GG, AG, and AA). *: P < 0.05, ns: not significant, Mann–Whitney U test. f Difference in expression of ARL4C in three groups of GC patients with different SNP rs1464264 genotypes (GG, AG, and AA) in the Singapore cohort (n= 161). *: P < 0.05, ns: not significant, Student’s t test. g Survival analysis comparing patient groups with samples exhibiting low (green) and high (red) expression of ARL4C in the ACRG cohort (n = 300). P value is calculated using the Log-rank test. Survival data are indicated for every 25 months

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