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Differential effects of estrogen receptor beta isoforms on glioblastoma progression

ABSTRACT: We examined the transcriptional changes modulated by knocking out ERβ and reintroduction of ERβ1 and ERβ5 isoforms by perfroming global transcriptome analysis. ERβ was knocked out in U87 cells using CRISPR/Cas9 system and reintroduced the ERβ1 and ERβ5 isoforms in knockout background. RNA was isolated from control U87, U87-ERβ-KO, U87-ERβ1 and U87-ERβ5 cells and utilized for RNA-seq analysis. Our results demonstrated that ERβ-KO, ERβ1 and ERβ5 modulated unique pathways including NF-κB singaling, Jak/STAT pathway and mTOR signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE104296 | GEO | 2018/04/10

REPOSITORIES: GEO

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Estrogen receptor beta enhances chemotherapy response of GBM cells by down regulating DNA damage response pathways

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Overlapping and distinct functions between ERα and ERβ homodimers and corresponding transcriptomes in the same cellular context

Project description:The two estrogen receptors, ERα and ERβ function as ligand-inducible transcription factors. Most in vitro studies have reported that ERα drives breast cancer growth whereas ERβ, if expressed, suppresses growth. To dissect function and gene expression profile regulated by ERα or ERβ, respectively, we generated a novel cell model expressing only ERβ, by applying CRISPR-cas9 to delete ERα in MCF7 cells with stable Tet-Off-inducible ERβ expression. This model with ERβ expression only, exhibited regulation of known estrogen responsive genes in a ligand-dependent manner. By cell proliferation assay, we found that either ER was required for proliferation, and that while E2 increased proliferation of ERα (only) MCF7, it reduced proliferation of ERβ (only) MCF7 cells. RNA-Seq analysis revealed 768 and 984 specific target genes regulated by ERα and ERβ in response to E2, respectively. Furthermore, functional enrichment analysis showed that the two ER isoforms regulated cell proliferation in opposite direction. In conclusion, within the same cellular context the two ERs regulated cell proliferation in opposite manner by regulating distinct sets of target genes in response to E2. The novel developed cell model provides a novel and valuable resource to further complement the mechanistic understanding of the two different ER isoforms.

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Project description:Estrogen receptor beta (ERβ) is a ligand inducible transcription factor regulating gene expression in response to the female sex hormone estrogen. Previously, we found that ERβ deficiency results in changes in DNA methylation patterns at two gene promoters, implicating an involvement of ERβ in DNA methylation. In this study, we set out to explore this involvement on a genome-wide level, and to investigate the underlying mechanisms of this function. Using reduced representation bisulfite sequencing (RRBS), we compared genome-wide DNA methylation in mouse embryonic fibroblasts (MEFs) derived from wildtype (wt) and ERβ knock-out (βerko) mice, and identified around 8000 differentially methylated positions (DMPs). This suggests that ERβ is involved in regulating DNA methylation at specific sites in the genome.

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