The PRC2 molecule EED is a target of epigenetic therapy for neuroblastoma

Epigenetic modifications by polycomb repressive complex (PRC) molecules appear to play a role in the tumorigenesis and aggressiveness of neuroblastoma (NB). Embryonic ectoderm development (EED) is a member of the PRC2 complex that binds to the H3K27me3 mark deposited by EZH2 via propagation on adjac...

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Published inEuropean journal of cell biology Vol. 101; no. 3; p. 151238
Main Authors Shaliman, Dilibaerguli, Takenobu, Hisanori, Sugino, Ryuichi P., Ohira, Miki, Kamijo, Takehiko
Format Journal Article
LanguageEnglish
Published Germany Elsevier GmbH 01.06.2022
Elsevier
Subjects
Cell Proliferation - genetics
EED
Epigenesis, Genetic
Histone code
Humans
N-Myc Proto-Oncogene Protein - genetics
N-Myc Proto-Oncogene Protein - metabolism
Neuroblastoma
Neuroblastoma - drug therapy
Neuroblastoma - genetics
Neuroblastoma - metabolism
Polycomb
Polycomb Repressive Complex 2 - genetics
Polycomb Repressive Complex 2 - metabolism
Polycomb
Neuroblastoma
EED
Histone code
Online AccessGet full text

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Abstract Epigenetic modifications by polycomb repressive complex (PRC) molecules appear to play a role in the tumorigenesis and aggressiveness of neuroblastoma (NB). Embryonic ectoderm development (EED) is a member of the PRC2 complex that binds to the H3K27me3 mark deposited by EZH2 via propagation on adjacent nucleosomes. We herein investigated the molecular roles of EED in MYCN-amplified NB cells using EED-knockdown (KD) shRNAs, EED-knockout sgRNAs, and the EED small molecule inhibitor EED226. The suppression of EED markedly inhibited NB cell proliferation and flat and soft agar colony formation. A transcriptome analysis using microarrays of EED-KD NB cells indicated the de-repression of cell cycle-regulated and differentiation-related genes. The results of a GSEA analysis suggested that inhibitory cell cycle-regulated gene sets were markedly up-regulated. Furthermore, an epigenetic treatment with the EED inhibitor EED226 and the HDAC inhibitors valproic acid/SAHA effectively suppressed NB cell proliferation and colony formation. This combined epigenetic treatment up-regulated cell cycle-regulated and differentiation-related genes. The ChIP sequencing analysis of histone codes and PRC molecules suggested an epigenetic background for the de-repression of down-regulated genes in MYCN-amplified/PRC2 up-regulated NB. •Suppression of EED markedly inhibited NB cell proliferation/colony formation.•EED repressed differentiation-related and cell cycle arrest/death control genes as an important molecule of PRC2 complex.•EED inhibition and HDAC inhibitor effectively suppressed NB cell proliferation.
AbstractList Epigenetic modifications by polycomb repressive complex (PRC) molecules appear to play a role in the tumorigenesis and aggressiveness of neuroblastoma (NB). Embryonic ectoderm development (EED) is a member of the PRC2 complex that binds to the H3K27me3 mark deposited by EZH2 via propagation on adjacent nucleosomes. We herein investigated the molecular roles of EED in MYCN-amplified NB cells using EED-knockdown (KD) shRNAs, EED-knockout sgRNAs, and the EED small molecule inhibitor EED226. The suppression of EED markedly inhibited NB cell proliferation and flat and soft agar colony formation. A transcriptome analysis using microarrays of EED-KD NB cells indicated the de-repression of cell cycle-regulated and differentiation-related genes. The results of a GSEA analysis suggested that inhibitory cell cycle-regulated gene sets were markedly up-regulated. Furthermore, an epigenetic treatment with the EED inhibitor EED226 and the HDAC inhibitors valproic acid/SAHA effectively suppressed NB cell proliferation and colony formation. This combined epigenetic treatment up-regulated cell cycle-regulated and differentiation-related genes. The ChIP sequencing analysis of histone codes and PRC molecules suggested an epigenetic background for the de-repression of down-regulated genes in MYCN-amplified/PRC2 up-regulated NB.
Epigenetic modifications by polycomb repressive complex (PRC) molecules appear to play a role in the tumorigenesis and aggressiveness of neuroblastoma (NB). Embryonic ectoderm development (EED) is a member of the PRC2 complex that binds to the H3K27me3 mark deposited by EZH2 via propagation on adjacent nucleosomes. We herein investigated the molecular roles of EED in MYCN-amplified NB cells using EED-knockdown (KD) shRNAs, EED-knockout sgRNAs, and the EED small molecule inhibitor EED226. The suppression of EED markedly inhibited NB cell proliferation and flat and soft agar colony formation. A transcriptome analysis using microarrays of EED-KD NB cells indicated the de-repression of cell cycle-regulated and differentiation-related genes. The results of a GSEA analysis suggested that inhibitory cell cycle-regulated gene sets were markedly up-regulated. Furthermore, an epigenetic treatment with the EED inhibitor EED226 and the HDAC inhibitors valproic acid/SAHA effectively suppressed NB cell proliferation and colony formation. This combined epigenetic treatment up-regulated cell cycle-regulated and differentiation-related genes. The ChIP sequencing analysis of histone codes and PRC molecules suggested an epigenetic background for the de-repression of down-regulated genes in MYCN-amplified/PRC2 up-regulated NB. •Suppression of EED markedly inhibited NB cell proliferation/colony formation.•EED repressed differentiation-related and cell cycle arrest/death control genes as an important molecule of PRC2 complex.•EED inhibition and HDAC inhibitor effectively suppressed NB cell proliferation.
ArticleNumber 151238
Author Kamijo, Takehiko
Takenobu, Hisanori
Ohira, Miki
Shaliman, Dilibaerguli
Sugino, Ryuichi P.
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Issue 3
Keywords Polycomb
Neuroblastoma
EED
Histone code
Language English
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Snippet Epigenetic modifications by polycomb repressive complex (PRC) molecules appear to play a role in the tumorigenesis and aggressiveness of neuroblastoma (NB)....
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StartPage 151238
SubjectTerms Cell Proliferation - genetics
EED
Epigenesis, Genetic
Histone code
Humans
N-Myc Proto-Oncogene Protein - genetics
N-Myc Proto-Oncogene Protein - metabolism
Neuroblastoma
Neuroblastoma - drug therapy
Neuroblastoma - genetics
Neuroblastoma - metabolism
Polycomb
Polycomb Repressive Complex 2 - genetics
Polycomb Repressive Complex 2 - metabolism
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Title The PRC2 molecule EED is a target of epigenetic therapy for neuroblastoma
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