ArticleGenes & cancer2014
Functional antagonism of TMPRSS2-ERG splice variants in prostate cancer.
Article in Genes & cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Identification and characterization of novel ETV4 splice variants in prostate cancer.Scientific reports · 2023Article
- Androgen-Driven Fusion Genes and Chimeric Transcripts in Prostate Cancer.Frontiers in cell and developmental biology · 2021Review
- Molecular profiling of radical prostatectomy tissue from patients with no sign of progression identifiesOncotarget · 2019Article
- Calcium and Nuclear Signaling in Prostate Cancer.International journal of molecular sciences · 2018Review
- Noninvasive Prenatal Diagnosis Significance of ERG Methylation as a Biomarker in Down's Syndrome.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
- Regulation of endothelial homeostasis, vascular development and angiogenesis by the transcription factor ERG.Vascular pharmacology · 2016Review
- Autoantibodies against oncogenic ERG protein in prostate cancer: potential use in diagnosis and prognosis in a panel with C-MYC, AMACR and HERV-K Gag.Genes & cancer · 2016Article
- Molecular pathological epidemiology in diabetes mellitus and risk of hepatocellular carcinoma.World journal of hepatology · 2016Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
The fusion between ERG coding sequences and the TMPRSS2 promoter is the most prevalent in prostate cancer (CaP). The presence of two main types of TMPRSS2-ERG fusion transcripts in CaP specimens, Type I and Type II, prompted us to hypothesize that the cumulative actions of different ERG variants may impact CaP development/progression. Using TMPRSS2-ERG3 (Type I) and TMPRSS2-ERG8 (Type II) expression vectors, we determined that the TMPRSS2- ERG8 encoded protein is deficient in transcriptional regulation compared to TMPRSS2-ERG3. Co-transfection of vectors resulted in decreased transcriptional regulation compared to TMPRSS2-ERG3 alone, suggesting transdominance of ERG8. Expression of exogenous ERG8 protein resulted in a decrease in endogenous ERG3 protein levels in TMPRSS2-ERG positive VCaP cells, with a concomitant decrease in C-MYC. Further, we showed a physical association between ERG3 and ERG8 in live cells by the bimolecular fluorescence complementation assay, providing a basis for the observed effects. Inhibitory effects of TMPRSS2-ERG8 on TMPRSS2- ERG3 were also corroborated by gene expression data from human prostate cancers, which showed a positive correlation between C-MYC expression and TMPRSS2-ERG3/TMPRSS2- ERG8 ratio. We propose that an elevated TMPRSS2-ERG3/TMPRSS2-ERG8 ratio results in elevated C-MYC in CaP, providing a strong rationale for the biomarker and therapeutic utility of ERG splice variants, along with C-MYC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.