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Co-expression of genes with ERG in prostate cancers

ABSTRACT: ERG overexpression is the most frequent molecular alteration in prostate cancer. We analyzed different stages of prostate cancer to identify genes that were coexpressed with ERG overexpression. In primary prostate tumors, it was shown that TDRD1 expression was the strongest correlated gene with ERG overexpression and we suggest TDRD1 as a direct ERG target gene.

ORGANISM(S): Homo sapiens

PROVIDER: GSE41408 | GEO | 2013/02/11

SECONDARY ACCESSION(S): PRJNA177575

REPOSITORIES: GEO

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Co-expression of genes with ERG in prostate cancers

Project description:ERG overexpression is the most frequent molecular alteration in prostate cancer. We analyzed different stages of prostate cancer to identify genes that were coexpressed with ERG overexpression. In primary prostate tumors, it was shown that TDRD1 expression was the strongest correlated gene with ERG overexpression and we suggest TDRD1 as a direct ERG target gene. 48 Prostate cancer samples from radical prostatectomies were included in this study. These samples contained more than 70% cancer and less than 30% stromal tissue. Each sample was analyzed once.

2013-02-11 | E-GEOD-41408 | biostudies-arrayexpress

Co-expression of genes with ERG in prostate cancer cell lines

2013-02-11 | GSE41407 | GEO

Co-expression of genes with ERG in prostate cancer cell lines

Project description:ERG overexpression is the most frequent molecular alteration in prostate cancer. We analyzed different stages of prostate cancer to identify genes that were coexpressed with ERG overexpression. In primary prostate tumors, it was shown that TDRD1 expression was the strongest correlated gene with ERG overexpression and we suggest TDRD1 as a direct ERG target gene. 6 Prostate cancer cell lines and 11 prostate cancer xenografts are included in this study. Each sample was analyzed once.

2013-02-11 | E-GEOD-41407 | biostudies-arrayexpress

TMPRSS2-ERG and gain-of-function p53 mutants co-dictate pyrimidine synthesis and prostate cancer fitness [ERG and p53 ChIP-seq]

Project description:TMPRSS2-ERG fusion is the most common genetic alteration in prostate cancer (PCa) and TP53 is the most frequently mutated gene in human cancers. However, their precise roles in PCa pathogenesis remain elusive. Here we showed that TMPRSS2-ERG fusion co-occurred with TP53 deletion/mutation in PCa patient specimens. ERG overexpression and Trp53 knockout/R172H mutant knockin induced pyrimidine synthesis gene (PSG) expression and prostate tumorigenesis in mice. Gain-of-function p53 mutants bound to the CTNNB1 promoter and upregulated β-Catenin. Overexpressed ERG and β-Catenin co-occupied PSG loci and mediated PSG expression, and high PSG expression associated with increased β-Catenin level and poor overall survival of PCa patients. β-Catenin inhibition by proteolysis-targeting chimeras (PROTACs) of its co-activator CBP and partner proteins LEF1/TCFs blocked ERG/p53-mutant PCa growth. Our study identifies CTNNB1 as a transcriptional target of p53 GOF-mutants, and reveals a druggable dependency on β-Catenin and pyrimidine synthesis in p53-mutated cancers with or without TMPRSS2-ERG fusion.

2023-06-27 | GSE184623 | GEO

TMPRSS2-ERG and gain-of-function p53 mutants co-dictate pyrimidine synthesis and prostate cancer fitness [RNA-seq-2018 ERG-p53 project]

2023-06-27 | GSE184624 | GEO

TMPRSS2-ERG and gain-of-function p53 mutants co-dictate pyrimidine synthesis and prostate cancer fitness [RNA-seq-2021 ERG-p53 project]

2023-06-27 | GSE184625 | GEO

An AR-ERG co-mediated chromatin interactome defines the transcriptional network in prostate cancer cells

Project description:An aberrant androgen receptor (AR) transcriptional network underpins prostate cancer development. Even though the AR cistrome had been extensively studied in prostate cancers, information pertaining to the spatial architecture of the AR transcriptional circuitry remains limited due to the absence of an AR-associated chromatin interactome map. To resolve this, we utilized chromatin interaction analysis by paired-end tag (ChIA-PET) sequencing to profile AR-associated and ERG-associated long range chromatin interactions in an ERG fusion positive prostate cancer cell line. We identified ERG-associated long range chromatin interactions as an elemental component in the AR-associated chromatin interactome, acting in concert, to achieve coordinated regulation of AR target genes. In addition, we characterized the epigenetic signature of the AR/ERG anchor binding sites and implicated AR and ERG associated chromatin loopings for facilitating fusion gene formation in prostate cancers. Taken together, our results revealed the presence of an AR/ERG defined higher order chromatin structure exploited for driving prostate cancer progression.

2018-12-14 | GSE54946 | GEO

ERG is a critical regulator of Wnt/LEF1 signaling in prostate cancer

Project description:Chromosomal translocations juxtaposing the androgen-responsive TMPRSS2 promoter with the ETS-family transcription factor ERG result in aberrant ERG up-regulation in approximately 50% of prostate cancers. Studies to date have demonstrated important roles of ERG in inducing oncogenic properties of prostate cancer. Its molecular mechanisms of action, however, are yet to be fully understood. To address these questions, we generated engineered LNCaP cells with ERG overexpression followed by LEF1 knockdown as well as control cell lines. To further investigate the role of LEF1 in ERG fusion positive samples, we also knockdown ERG in VCaP cell line. We performed microarray analysis on LNCaP cells with ERG overexpression followed by LEF1 knockdown using siRNA. We also knockdown endogenous ERG in fusion-positive cell line VCaP.

2013-05-29 | E-GEOD-47423 | biostudies-arrayexpress

Staphylococcal Nuclease and Tudor Domain Containing protein SND1 interacts with ERG and plays a critical role in prostate cancer in vivo

Project description:ERG is a transcriptional factor, which is recombined with promoter of TMPRSS2 and prominently overexpressed in half of human prostate cancers. The mechanisms of ERG-mediated oncogenesis are not completely understood. We performed an unbiased Mass Spectrometry screen for ERG-binding proteins and found that ERG binds to MTDH/SND1 protein complex in prostate cancer cells. We determined that ERG binds to the SND1/MTDH protein complex via SND1 and this interaction plays a critical role in ERG-mediated cancer.

2023-03-22 | PXD036882 | Pride

Genomic profiling of H3K27ac and transcription factor binding in ERG-overexpressing prostate cancer

Project description:Structural rearrangements leading to the TMPRSS2:ERG (T2E) fusion typify ~50% of prostate tumors and result in overexpression of the ERG transcription factor. Using T2E and non-T2E primary prostate tumors, we assessed the impact of ERG overexpression on chromatin by integrating ChIP-seq against H3K27ac, a chromatin modification found at active cis-regulatory elements, with paired genomic and expression data. We show that T2E tumors have a consistent and distinct cis-regulatory landscape to non-T2E tumors which drives their unique transcriptional profile. The T2E-specific cis-regulatory landscape is driven by ERG-mediated co-option of prostate master transcription factors HOXB13 and FOXA1 and is typified by Cluster Of Regulatory Elements (COREs) including one spreading into the ERG locus of the structurally rearranged allele. This gives rise to a cis-regulatory element within the rearranged ERG gene that contributes to ERG overexpression. The unique cis-regulatory landscape in T2E primary prostate tumors also reveals the activation of the NOTCH signalling pathway. Accordingly, chemical NOTCH pathway inhibition limited the invasive nature of T2E prostate cancer cells, revealing an actionable vulnerability against T2E prostate tumors. Taken together, our work delineates the role of ERG over-expression in co-opting master transcription factors to deploy a unique cis-regulatory landscape inducing a dependency on NOTCH signaling in T2E prostate tumors.

2017-07-25 | GSE96652 | GEO

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