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Fig. 6 | Genome Medicine

Fig. 6

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

Fig. 6

Trans-analysis of differential enhancers. a Top 5 transcription factor binding enrichments at SNU16-specific enhancers determined by HOMER de novo motif analysis. The last column shows the percentage of target sequence with the corresponding motif. b Expression of HNF4α in normal gastric (n = 89) and GC samples (n = 185) from the Singapore cohort. Expression of HNF4α in normal gastric (n = 35) and GC samples (n = 415) from the TCGA cohort. P value: Mann–Whitney U test. c Integration of H3K27ac ChIP-seq data, HNF4α ChIP-seq binding profiles (SNU16, YCC3, IM95, KATOIII, IST1, NUGC4, and OCUM1) and RNA-seq data in control, HNF4α overexpressing cells (HFE145), HNF4α knockdown (YCC3) at the GRHL2 gene locus. The red box indicates an enhancer associated with GRHL2 (chr8: 102,449,130-102,450,795). d GRHL2 gene expression levels and H3K27ac signals over the enhancer for GRHL2 are linearly correlated across 28 cell lines. R: Pearson’s correlation coefficient. P value: Pearson’s correlation test. e Singapore cohort analysis reveals GRHL2 and HNF4α transcriptomic correlations using microarray data (Pearson’s correlation test). f TCGA cohort analysis confirms GRHL2 and HNF4α transcriptomic correlations using RNA-seq data (Pearson’s correlation test)

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