Microsatellite enhancers can be targeted to impair tumorigenesis

Dysregulation of repetitive elements has been implicated in many cancers and other human diseases; however, the role of repetitive elements remains largely unexplored. In this issue of Genes & Development, Boulay and colleagues (pp. 1008–1019) explore the ability of GGAA repeats to act as altern...

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Detalles Bibliográficos
Autores principales: Kaeding, Kelsey E., Zaret, Kenneth S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cold Spring Harbor Laboratory Press 2018
Materias:
Outlook
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6075152/
https://www.ncbi.nlm.nih.gov/pubmed/30068701
http://dx.doi.org/10.1101/gad.318105.118
Descripción
Sumario:Dysregulation of repetitive elements has been implicated in many cancers and other human diseases; however, the role of repetitive elements remains largely unexplored. In this issue of Genes & Development, Boulay and colleagues (pp. 1008–1019) explore the ability of GGAA repeats to act as alternative enhancers activated by EWS-FLI1 in Ewing sarcoma and contribute to tumorigenesis. Using CRISPR-mediated epigenome editing, repression of EWS-FLI1 targeted microsatellite enhancers halted aberrant gene expression and impaired the growth of Ewing sarcoma xenografts in vivo. The study reveals the regulatory capacity of repetitive elements in cancer and offers insight into therapeutic targets for Ewing sarcoma.

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