EED regulates epithelial-mesenchymal transition of cancer cells induced by TGF-ß.
Biochem Biophys Res Commun
; 453(1): 124-30, 2014 Oct 10.
Article
en En
| MEDLINE
| ID: mdl-25264103
ABSTRACT
Histone methylation is involved in various biological and pathological processes including cancer development. In this study, we found that EED, a component of Polycomb repressive complex-2 (PRC2) that catalyzes methylation of lysine 27 of histone H3 (H3K27), was involved in epithelial-mesenchymal transition (EMT) of cancer cells induced by Transforming Growth Factor-beta (TGF-ß). The expression of EED was increased during TGF-ß-induced EMT and knockdown of EED inhibited TGF-ß-induced morphological conversion of the cells associated with EMT. EED knockdown antagonized TGF-ß-dependent expression changes of EMT-related genes such as CDH1, ZEB1, ZEB2 and microRNA-200 (miR-200) family. Chromatin immunoprecipitation assays showed that EED was implicated in TGF-ß-induced transcriptional repression of CDH1 and miR-200 family genes through the regulation of histone H3 methylation and EZH2 occupancies on their regulatory regions. Our study demonstrated a novel role of EED, which regulates PRC2 activity and histone methylation during TGF-ß-induced EMT of cancer cells.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Factor de Crecimiento Transformador beta
/
Transición Epitelial-Mesenquimal
/
Complejo Represivo Polycomb 2
/
Neoplasias
Límite:
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2014
Tipo del documento:
Article
País de afiliación:
Japón