ArticleOncotarget2017
TMPRSS2:ERG gene fusion variants induce TGF-β signaling and epithelial to mesenchymal transition in human prostate cancer cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- 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
- Transient Receptor Potential Channels in Prostate Cancer: Associations with ERG Fusions and Survival.International journal of molecular sciences · 2025Article
- Construction of gastric cancer prognostic signature based on the E26 transcription factor and the identification of novel oncogene ELK3.American journal of cancer research · 2024Article
- Review
- Infection by High-Risk Human Papillomaviruses, Epithelial-to-Mesenchymal Transition and Squamous Pre-Malignant or Malignant Lesions of the Uterine Cervix: A Series of Chained Events?International journal of molecular sciences · 2021Review
- Ras/ERK and PI3K/AKT signaling differentially regulate oncogenic ERG mediated transcription in prostate cells.PLoS genetics · 2021Article
- Article
- Mutational drivers of cancer cell migration and invasion.British journal of cancer · 2021Review
- Upregulation of the heterogeneous nuclear ribonucleoprotein hnRNPA1 is an independent predictor of early biochemical recurrence in TMPRSS2:ERG fusion-negative prostate cancers.Virchows Archiv : an international journal of pathology · 2020Article
- Ras and Wnt Interaction Contribute in Prostate Cancer Bone Metastasis.Molecules (Basel, Switzerland) · 2020Review
- Exome sequencing identified six copy number variations as a prediction model for recurrence of primary prostate cancers with distinctive prognosis.Translational cancer research · 2020Article
- Article
- Comparative RNA-seq analysis reveals dys-regulation of major canonical pathways in ERG-inducible LNCaP cell progression model of prostate cancer.Oncotarget · 2019Article
- The Reduced PC-Algorithm: Improved Causal Structure Learning in Large Random Networks.Journal of machine learning research : JMLR · 2019Article
- Genome-Based Classification and Therapy of Prostate Cancer.Diagnostics (Basel, Switzerland) · 2018Review
- Systematic analysis reveals molecular characteristics of ERG-negative prostate cancer.Scientific reports · 2018Article
- High expression of hnRNPA1 promotes cell invasion by inducing EMT in gastric cancer.Oncology reports · 2018Article
- Oncogenic fusion proteins adopt the insulin-like growth factor signaling pathway.Molecular cancer · 2018Review
- Overexpression of lncRNA ANRIL promoted the proliferation and migration of prostate cancer cells via regulating let-7a/TGF-β1/ Smad signaling pathway.Cancer biomarkers : section A of Disease markers · 2018Article
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TMPRSS2:ERG (T/E) gene fusions are present in approximately 50% of all prostate cancer (PCa) cases. The expression of fusion mRNAs from distinct T/E variants is associated with clinicopathological parameters, while the underlying molecular processes remain unclear. We characterized the molecular mechanisms and functional implications caused by doxycycline (Dox)-inducible overexpression of the frequent T/E III and VI fusion variants in LNCaP cells. Induction of T/E expression resulted in increased cellular migratory and invasive potential, and reduced proliferation and accumulation in G1 phase. T/E overexpressing cells showed epithelial-to-mesenchymal transition (EMT), as demonstrated by upregulation of TGF-β and WNT pathway genes, mesenchymal markers, and increased phosphorylation of the p38 MAPK. Augmented secretion of TGF-β1 and -β2, and T/E-mediated regulation of ALK1, a member of the TGF-β receptor family, was detected. ALK1 inhibition in T/E overexpressing cells blocked p38 phosphorylation and reduced the expression of the TGF-β target genes VIM, MMP1, CDH2, and SNAI2. We found a T/E variant VI-specific induction of miR-503 associated with reduced expression of SMAD7 and CDH1. Overexpression of miR-503 led to increased levels of VIM and MMP1. Our findings indicate that TGF-β signaling is a major determinant of EMT in T/E overexpressing LNCaP cells. We provide evidence that T/E VI-specific transcriptional modulation by miR-503 accounts for differences in the activation of EMT pathway genes, promoting the aggressive phenotype of tumors expressing T/E variant VI. We suggest that ALK1-mediated TGF-β signaling is a novel oncogenic mechanism in T/E positive PCa.
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