Journal
BIOMEDICINES
Volume 10, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines10061325
Keywords
Ewing sarcoma; fusion protein; EWSR1-FLI1; EWS-FLI1; epigenetic regulation; transcriptional regulation; functional genomic screens; high throughput screens
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Funding
- Alex's Lemonade Stand Foundation Innovation Award [18-11849]
- Stand Up to Cancer-Cancer Research UK Pediatric Cancer New Discoveries Challenge Award [RT6187]
- National Institutes of Health [R37 CA233691, R01 CA236626]
- Sarcoma Foundation of America [2022 SFA 05-22]
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This review discusses the epigenetic and transcriptional alterations in Ewing sarcoma and summarizes the relevant screening studies conducted to develop novel therapies.
Ewing sarcoma (EwS), a type of bone and soft tissue tumor, is mainly driven by the expression of the fusion protein EWSR1-FLI1. Upon binding to chromatin, EWSR1-FLI1 reprograms the epigenetic state, alters gene expression, and thus leads to tumorigenesis. Considerable studies have investigated the epigenomic and transcriptomic profiling of EwS. Nevertheless, a comprehensive view of therapeutic targets is still lacking. This review discusses the epigenetic and transcriptional alterations reported in EwS. Specifically, we discuss the binding characteristics of EWSR1-FLI1 on chromatin, the mechanisms of EWSR1-FLI1 in reprograming epigenome, and EWSR1-FLI1-induced transcriptional alterations. Moreover, we summarize the chemical, RNAi, and CRISPR-cas9 high throughput screens conducted in EwS with the goal of assisting in the development of novel therapies to treat this aggressive disease.
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