Enhancer ID: | E_02_0858 |
Species: | human |
Position : | chr3:186938165-186940165 |
Biosample name: | |
Experiment class : | Low+High throughput |
Enhancer type: | Super-Enhancer |
Disease: | B-cell lymphoma |
Pubmed ID: | 26229090 |
Enhancer experiment: | ChIP-seq,3C,qRT-PCR |
Enhancer experiment description: | This highlighted a known BCL6-interacting Enhancer region (6,16,17) 150-250 upstream of BCL6 (SE1),which overlaps the alternate breakpoint region,a recurrent site of BCL6 locus rearrangements (15). It also revealed a second Super-Enhancer overlapping the HGB-04 duplication at ?350 (SE2),and a third such region at ?500 (SE3).We used chromosome conformation capture (3C) analysis of GCB-DLBCL lymphoma cell lines (Supplementary Fig. S3A) to confirm looping of elements from super-enhancer regions to the BCL6 promoter, consistent with roles in activating this oncogene. Intriguingly, our PMBL case, HGB-04, showed a distinct acetylation pattern across these regions, with only the duplicated enhancer region, SE2, showing strong acetylation. In both cases, we detected the expected interactions between the BCL6 and MYC promoters and candidate enhancers in their native locus (Fig. 5C-D). We then used the same enhancer primers to measure interactions with the opposite gene promoter. We detected strong interactions between the MYC promoter and elements within the BCL6 SE1 and SE2 regions in HGB-07, but no such interactions in the non-rearranged tumor, HGB-06. |
Target gene : | BCL6(BCL5A,LAZ3,ZBTB27,ZNF51,BCL6) |
Strong evidence: | 3C |
Less strong evidence: | qRT-PCR |
Target gene experiment description: | This highlighted a known BCL6-interacting Enhancer region (6,16,17) 150-250 upstream of BCL6 (SE1),which overlaps the alternate breakpoint region,a recurrent site of BCL6 locus rearrangements (15). It also revealed a second Super-Enhancer overlapping the HGB-04 duplication at ?350 (SE2),and a third such region at ?500 (SE3).We used chromosome conformation capture (3C) analysis of GCB-DLBCL lymphoma cell lines (Supplementary Fig. S3A) to confirm looping of elements from super-enhancer regions to the BCL6 promoter, consistent with roles in activating this oncogene. Intriguingly, our PMBL case, HGB-04, showed a distinct acetylation pattern across these regions, with only the duplicated enhancer region, SE2, showing strong acetylation. In both cases, we detected the expected interactions between the BCL6 and MYC promoters and candidate enhancers in their native locus (Fig. 5C-D). We then used the same enhancer primers to measure interactions with the opposite gene promoter. We detected strong interactions between the MYC promoter and elements within the BCL6 SE1 and SE2 regions in HGB-07, but no such interactions in the non-rearranged tumor, HGB-06. |
TF name : | MEF2B(MEF2B) |
TF experiment: | ChIP-Seq |
TF experiment description: | Rather, we observed strong, focal MEF2B binding at acetylated elements within BCL6 super-enhancer regions, including four sites in SE1, one in SE2, and two in SE3 (Fig. 3C). ChIP-Seq analysis in the Jeko-1 MCL line revealed a specific increase in H3K27ac at MEF2B binding sites in MEF2B transgene-expressing cells, but not at intervening elements within the BCL6 super-enhancers (Fig. 3E).These data support a direct role for MEF2B in the activation of enhancers that drive BCL6 expression in human lymphomas. |
Enhancer function : | -- |
Enhancer function experiment: | -- |
Enhancer function experiment description: |
-- |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
---|---|---|---|
MEF2B | CDO in myogenesis | reactome | 29 |
MEF2B | p38 MAPK pathway | panther | 31 |