ArticlePLoS genetics2021
Ras/ERK and PI3K/AKT signaling differentially regulate oncogenic ERG mediated transcription in prostate cells.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- ERG Orchestrates a Dedifferentiation-Senescence-Inflammation Triad in Prostate Cancer.Molecular cancer research : MCR · 2026Article
- ERG function in prostate cells is regulated by distinct positive feedback loops depending on AKT signaling status.Research square · 2026Article
- Multiple ETS family transcription factors bind mutant p53 via distinct interaction regions.FEBS letters · 2026Article
- NLRX1 Drives Prostate Cancer Progression Through Activation of AKT and ERK Signaling Pathways.International journal of biological sciences · 2026Article
- DeeP4med: deep learning for P4 medicine to predict normal and cancer transcriptome in multiple human tissues.BMC bioinformatics · 2023Article
- Article
- From Omics to Multi-Omics Approaches for In-Depth Analysis of the Molecular Mechanisms of Prostate Cancer.International journal of molecular sciences · 2022Review
- The Expression of Proto-OncogeneInternational journal of molecular sciences · 2022Review
- Review
- IPO5 Mediates EMT and Promotes Esophageal Cancer Development through the RAS-ERK Pathway.Oxidative medicine and cellular longevity · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The TMPRSS2/ERG gene rearrangement occurs in 50% of prostate tumors and results in expression of the transcription factor ERG, which is normally silent in prostate cells. ERG expression promotes prostate tumor formation and luminal epithelial cell fates when combined with PI3K/AKT pathway activation, however the mechanism of synergy is not known. In contrast to luminal fates, expression of ERG alone in immortalized normal prostate epithelial cells promotes cell migration and epithelial to mesenchymal transition (EMT). Migration requires ERG serine 96 phosphorylation via endogenous Ras/ERK signaling. We found that a phosphomimetic mutant, S96E ERG, drove tumor formation and clonogenic survival without activated AKT. S96 was only phosphorylated on nuclear ERG, and differential recruitment of ERK to a subset of ERG-bound chromatin associated with ERG-activated, but not ERG-repressed genes. S96E did not alter ERG genomic binding, but caused a loss of ERG-mediated repression, EZH2 binding and H3K27 methylation. In contrast, AKT activation altered the ERG cistrome and promoted expression of luminal cell fate genes. These data suggest that, depending on AKT status, ERG can promote either luminal or EMT transcription programs, but ERG can promote tumorigenesis independent of these cell fates and tumorigenesis requires only the transcriptional activation function.
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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.