Comprehensive Analysis of Chromatin States in Atypical Teratoid/Rhabdoid Tumor Identifies Diverging Roles for SWI/SNF and Polycomb in Gene Regulationстатья

Статья опубликована в высокорейтинговом журнале

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Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 3 февраля 2019 г.

Работа с статьей

[1] Comprehensive analysis of chromatin states in atypical teratoid/rhabdoid tumor identifies diverging roles for swi/snf and polycomb in gene regulation / S. Erkek, P. Johann, M. Finetti et al. // Cancer Cell. — 2019. — Vol. 35. — P. 95–110. VOLUME 35, ISSUE 1, P95-110.E8, JANUARY 14, 2019 Highlights • ATRT epigenomes display a global depletion of H3K27ac and H3K27me3 • Neuronal genes bound by SMARCB1 in normal brain are repressed by EZH2 in ATRT • ATRT harbor many active genes occupied by EZH2 but without occupancy of H3K27me3 • Residual SWI/SNF occupancy maintains genes active in the presence of Polycomb complex Summary Biallelic inactivation of SMARCB1, encoding a member of the SWI/SNF chromatin remodeling complex, is the hallmark genetic aberration of atypical teratoid rhabdoid tumors (ATRT). Here, we report how loss of SMARCB1 affects the epigenome in these tumors. Using chromatin immunoprecipitation sequencing (ChIP-seq) on primary tumors for a series of active and repressive histone marks, we identified the chromatin states differentially represented in ATRTs compared with other brain tumors and non-neoplastic brain. Re-expression of SMARCB1 in ATRT cell lines enabled confirmation of our genome-wide findings for the chromatin states. Additional generation of ChIP-seq data for SWI/SNF and Polycomb group proteins and the transcriptional repressor protein REST determined differential dependencies of SWI/SNF and Polycomb complexes in regulation of diverse gene sets in ATRTs. Keywords atypical teratoid rhabdoid tumor, pediatric brain tumor, SMARCB1, SMARCA4, EZH2, chromatin states. [ DOI ]

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