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ChIP-seq analysis of H4K12Ac antibody binding in hTert-HME1 cells treated with either control or BRCA2 siRNAs

ABSTRACT: Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function (“BRCA2-crisis”), which may contribute to disease. Here we establish an in vitro model for BRCA2-crisis that demonstrates novel epigenetic remodeling and activation of an NF-κB survival pathway in response to transient BRCA2-depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These epigenetic alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2-carriers and therefore may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE133728 | GEO | 2019/08/07

REPOSITORIES: GEO

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BRCA2 ChIP-seq hTert-HME1 cell line

Project description:Individuals with a single functional copy of the BRCA2 tumor suppressor have elevated risks for breast, ovarian, and other solid tumor malignancies. The exact mechanisms of carcinogenesis due to BRCA2 haploinsufficiency remain unclear, but one possibility is that at-risk cells are subject to acute periods of decreased BRCA2 availability and function ("BRCA2-crisis"), which may contribute to disease. Here, we establish an in vitro model for BRCA2-crisis that demonstrates chromatin remodeling and activation of an NF-κB survival pathway in response to transient BRCA2 depletion. Mechanistically, we identify BRCA2 chromatin binding, histone acetylation, and associated transcriptional activity as critical determinants of the epigenetic response to BRCA2-crisis. These chromatin alterations are reflected in transcriptional profiles of pre-malignant tissues from BRCA2 carriers and, therefore, may reflect natural steps in human disease. By modeling BRCA2-crisis in vitro, we have derived insights into pre-neoplastic molecular alterations that may enhance the development of preventative therapies.

2019-08-07 | GSE133450 | GEO

Genome-wide mapping of DNA-methylation in hTert-HME1 cell line treated with control or BRCA2 siRNAs and grown with or without EGF (epithelial growth factor)

2019-08-07 | GSE107103 | GEO

Gene expression profiling by RNA-seq in hTert-HME1 cell line treated with control or BRCA2 siRNAs and grown with or without EGF (epithelial growth factor) II

2019-08-07 | GSE107280 | GEO

BRCA2 ChIP-seq hTert-HME1 cell line

Project description:BRCA2 ChIP-seq hTert-HME1 cell line

| PRJNA551474 | ENA

Gene expression profiling by RNA-seq in hTert-HME1 cell line treated with control or BRCA2 siRNAs and grown with or without EGF (epithelial growth factor)

Project description:Mammary epithelial cells were treated with control or BRCA2 siRNAs, then allowed to recover for 4 passages, then grown in mammary epithelial growth media supplemented with or without EGF (epithelial growth factor) for 2 passages (6 days).

2019-07-02 | GSE107121 | GEO

Genome-wide mapping of accessible chromatin in hTert-HME1 cell line treated with control or BRCA2 siRNAs and grown with or without EGF (epithelial growth factor)

Project description:Mammary epithelial cell line hTert-HME1 was transfected with Control or BRCA2 siRNAs then passaged four times (12 days), then were grown in mammary epithelial growth medium with or without EGF (epithelial growth factor) for 2 passages (6 days).

2019-07-02 | GSE107119 | GEO

ChIP-seq analysis of H4K12Ac antibody binding in hTert-HME1 cells treated with either control or BRCA2 siRNAs

Project description:ChIP-seq analysis of H4K12Ac antibody binding in hTert-HME1 cells treated with either control or BRCA2 siRNAs

| PRJNA552347 | ENA

Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers

Project description:This SuperSeries is composed of the following subset Series: GSE32124: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [expression data] GSE32258: Effects of BRCA2 cis-regulation in normal breast and cancer risk amongst BRCA2 mutation carriers [SNP data] Refer to individual Series

2012-02-01 | E-GEOD-32259 | biostudies-arrayexpress

BRCA2 abrogation triggers innate immune responses potentiated by treatment with PARP inhibitors

Project description:Heterozygous germline mutations in BRCA2 predispose to breast and ovarian cancer. Contrary to non-cancerous cells, where BRCA2 deletion causes cell cycle arrest or cell death, BRCA2 inactivation in tumors is associated with uncontrolled cell proliferation. We set out to investigate this conundrum by exploring modalities of cell adaptation to loss of BRCA2 and focused on genome-wide transcriptome alterations. Human cells in which BRCA2 expression was inhibited using a doxycycline (DOX)-inducible shRNA for 4 or 28 days were subjected to RNA-seq analyses. Gene sets differentially expressed in BRCA2-deficient versus -proficient cells revealed a biphasic response to BRCA2 abrogation. The early, acute response consisted of downregulation of genes involved in cell cycle progression, DNA replication and repair and was associated with cell cycle arrest in G1. Surprisingly, the late, chronic response consisted exclusively of upregulation of innate immune response genes controlled by interferon. Activation of the cGAS-STING pathway detected in these cells further substantiated the concept that long-term BRCA2 abrogation triggers cell-intrinsic immune signaling. Importantly, we found that treatment with PARP inhibitors stimulated the interferon response in cells and tumors lacking BRCA2. We propose that PARP inhibitors suppress growth of BRCA2-deficient cells and tumors, in part, by activating interferon signaling.

2018-12-11 | GSE123631 | GEO

ChIA-PET from hTERT-HME1 (ENCSR991JXX)

Project description:RAD21 ChIA-PET in human hTERT-HME1 cells For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf

2019-03-03 | GSE127054 | GEO

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