Correction for Wood et al., “Enhancer Control of MicroRNA miR-155 Expression in Epstein-Barr Virus-Infected B Cells”

Wood, C. David; Carvell, Thomas; Gunnell, Andrea; Ojeniyi, Opeoluwa O.; Osborne, Cameron S.; West, Michelle J.

doi:10.1128/jvi.01893-18

Cited by 3 publications

(2 citation statements)

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“…Previous studies have shown that enhancers can recruit TFs to positively promote target gene expression, and consequently cause HCC tumorigenesis [5]. Recent studies showed that enhancers (including typical enhancers and super enhancers) can regulate miRNA expression and participate in the biological synthesis by regulating Drosha/DGCR8 [6,7]. However, whether the regulatory network is formed by TEAD1, enhancer and microRNA and whether the regulatory network is involved in the regulation of HCC are unclear.…”

Section: Introductionmentioning

confidence: 99%

Identification and function of TEAD1 regulated enhancer in HepG2 cells

Tang

Zhang

Zhong

et al. 2022

Preprint

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Background Recent studies have shown that regulatory networks constituted by TFs, enhancer, and miRNAs is crucial for transcriptional regulation and progression in cancer. However, it is unclear whether TEAD1, a cancer-related transcription factor, is involved in enhancer-miRNA network and participates in tumorigenesis and development of hepatocellular carcinoma (HCC). Methods and Results In this study, we first identified 14,286 active enhancers through integrating CAGE-seq and GRO-seq of HepG2, and confirmed that these active enhancers have previously approved features. Moreover, 2,550 enhancers that bound by TEAD1 (EnhTEAD1) were identified through combining 35,883 TEAD1-DNA binding sites. Furthermore, in order to conveniently study the function of TEAD1-enhancer, we divided the enhancers into two categories by whether they are combined with TEAD1: EnhTEAD1 and Enhno-TEAD1. We found that the expression of eRNA (enhancer RNA) and markers of active enhancers (H3K27ac, H3K4me1 and H3K4me3) were significantly higher on EnhTEAD1 than on Enhno-TEAD1. In addition, we suggest that TEAD1 may function as a co-factor with several TFs (GATA4, HNF4A, YY1 and CTCF) and promotes chromosomal accessibility and spatial looping of EnhTEAD1. We performed the small RNA sequencing after interfering with TEAD1 by siRNA in the HCC HepG2 cells. Totally, 68 EnhTEAD1-regulated differently expressed miRNAs interactions (EnhTEAD1-miRNAs) were obtained by RNA-seq and Hi-C. Finally, we found that these EnhTEAD1-miRNAs were significantly involved in kinds of cancer-related pathways and biological processes . Conclusion In summary, this study elucidates the regulation mechanism of EnhTEAD1-miRNAs network in HCC, and also provides a new potential target for the further treatment of HCC.

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Section: Introductionmentioning

confidence: 99%

Identification and function of TEAD1 regulated enhancer in HepG2 cells

Tang

Zhang

Zhong

et al. 2022

Preprint

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“…A recent study showed that miR-24-1, which is present in the nucleus, promotes gene expression by targeting enhancers, suggesting that there is an obvious interaction between enhancers and miRNAs ( Xiao et al, 2017 ). Other recent studies showed that enhancers (including typical enhancers and super enhancers) are found to regulate miRNA expression and participate in the biological synthesis of miRNAs regulated by Drosha/DGCR8 ( Yun et al, 2018 ; Wood et al, 2019 ). These studies suggested that enhancers are involved in miRNA regulatory networks and contribute greatly to tumorigenesis and development.…”

Section: Introductionmentioning

confidence: 99%

Genome-Wide Identification and Analysis of Enhancer-Regulated microRNAs Across 31 Human Cancers

et al. 2020

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Enhancers are cis -regulatory DNA elements that positively regulate the transcription of target genes in a tissue-specific manner, and dysregulation of target genes could lead to various diseases, such as cancer. Recent studies have shown that enhancers can regulate microRNAs (miRNAs) and participate in their biological synthesis. However, the network of enhancer-regulated miRNAs across multiple cancers is still unclear. Here, a total of 2,418 proximal enhancer–miRNA interactions and 1,280 distal enhancer–miRNA interactions were identified through the integration of genomic distance, co-expression, and 3D genome data in 31 cancers. The results showed that both proximal and distal interactions exhibited a significant cancer type-specific feature trend at the tissue level rather than at the single-cell level, and there was a noteworthy positive correlation between the expression of the miRNA and the number of enhancers regulating the same miRNA in most cancers. Furthermore, we found that there was a high correlation between the formation of enhancer–miRNA pairs and the expression of enhancer RNAs (eRNAs) whether in distal or proximal regulation. The characteristics analysis showed that miRes (enhancers that regulated miRNAs) and non-miRes presented significant differences in sequence conservation, guanine–cytosine (GC) content, and histone modification signatures. Notably, GC content, H3K4me1, and H3K36me3 were present differently between distal and proximal regulation, suggesting that they might participate in chromosome looping of enhancer–miRNA interactions. Finally, we introduced a case study, enhancer: chr1:1186391–1186507 ∼ miR-200a was highly relevant to the survival of thyroid cancer patients and a cis -eQTL SNP on the enhancer affected the expression of the TNFRSF18 gene as a tumor suppressor.

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Genome-wide identification and analysis of enhancer regulated microRNAs across 31 human cancers

Tang

Lang

Wang

et al. 2020

Preprint

View full text Add to dashboard Cite

Enhancers are cis-regulatory DNA elements that positively regulate the transcription of target genes in a tissue-specific manner and dysregulation in various diseases such as cancer. Recent studies showed that enhancers can regulate miRNAs and participate in the biological synthesis of miRNAs. However, the network of enhancer-regulated miRNAs across multiple cancers is still unclear. Here, a total of 2,418 proximal enhancer-miRNA interactions and 1,280 distal enhancer-miRNA interactions were identified through the integration of genomic distance, co-expression, and 3D genome data in 31 cancers. The results showed that both proximal and distal interactions exhibited significant tissue-specific feature and there was a noteworthy positive correlation between the expression of miRNA and the number of regulated enhancers in most tissues. Furthermore, it was found that there was a high correlation between the formation of enhancer-miRNA pairs and the expression of eRNAs whether in distal or proximal regulation. The characteristics analysis showed that miRes (enhancers that regulated miRNAs) and non-miRes presented significant differences in sequence conservation, GC content and histone modification signatures. Notably, GC content, H3K4me1, H3K36me3 were present differently between distal regulation and proximal regulation, suggesting they might participate in chromosome looping of enhancer-miRNA interactions. Finally, we introduced a case study, enhancer: chr1:1186391-1186507~miR-200a was highly relevant to the survival of thyroid cancer patients and a cis-eQTL SNP on enhancer affected the expression TNFRSF18 gene as a tumor suppressor.

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Correction for Wood et al., “Enhancer Control of MicroRNA miR-155 Expression in Epstein-Barr Virus-Infected B Cells”

Cited by 3 publications

References 0 publications

Identification and function of TEAD1 regulated enhancer in HepG2 cells

Identification and function of TEAD1 regulated enhancer in HepG2 cells

Genome-Wide Identification and Analysis of Enhancer-Regulated microRNAs Across 31 Human Cancers

Genome-wide identification and analysis of enhancer regulated microRNAs across 31 human cancers

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