However, there is a scarcity of studies that systematically elucidated the role of SEs in HCC and its new prospects for therapeutic targets. Thus, this review summarizes the identification, formation and organization approaches of SEs, focusing on the mode of mechanism as well as the drug inhibito...
Here, we review the structural characteristics, organization, identification, and functions of SEs and the underlying molecular mechanism by which SEs drive oncogenic transcription in tumor cells. We then summarize abnormal SE complexes, SE-driven coding genes, and noncoding RNAs involved in tumor deve...
In mammalian cells, cell identity genes that are regulated by super-enhancers (SEs) are also densely occupied by transcriptional machinery that form phase-separated condensates. We suggest that the stress-remodeled yeast nucleome bears functional and structural resemblance to mammalian SEs, and will ...
BRD4, a member of the bromodomain and extraterminal domain protein (BET) family, plays a role in SE organization and oncogene expression regulation91. Mechanistically, BRD4 binds to acetylated lysines in enhancers, SEs, and TFs, bringing them together and mediating transcriptional activation and elon...
Super-enhancers (SEs), also known as stretch-enhancers, are a subset of enhancers especially important for genes associated with cell identity and genetic risk of disease2,3,4,5,6. CD4+ T cells are critical for host defence and autoimmunity. Here we analysed maps of mouse T-cell SEs as ...
Metastasis remains the principal cause of cancer-related lethality despite advancements in cancer treatment. Dysfunctional epigenetic alterations are crucial in the metastatic cascade. Among these, super-enhancers (SEs), emerging as new epigenetic regula
Metastasis remains the principal cause of cancer-related lethality despite advancements in cancer treatment. Dysfunctional epigenetic alterations are crucial in the metastatic cascade. Among these, super-enhancers (SEs), emerging as new epigenetic regula
Oncogenic SEs promote tumorigenesis and malignancy by altering protein-coding gene expression and noncoding regulatory element function. Therefore, they play central roles in the treatment of cancer. Here, we review the structural characteristics, organization, identification, and functions of SEs and the...
Mechanistically, we found that HMGB1 promoted the formation of super-enhancers (SEs) of CIITA, epigenetically reprogramming DCs and promoting trained immunity. The SEs inhibitor JQ1 reduced the expression of CIITA and MHC-II in DCs, thereby delaying the occurrence of chronic rejection. Interestingly,...
Transcription factors, cofactors, chromatin regulators, and transcription apparatuses interact with transcriptional regulatory elements, including promoters, enhancers, and super-enhancers (SEs), to coordinately regulate the transcription of target genes