ArticleScientific reports2019
hASH1 nuclear localization persists in neuroendocrine transdifferentiated prostate cancer cells, even upon reintroduction of androgen.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanistic insights and molecular therapy for neuroendocrine prostate cancer.Frontiers in oncology · 2026Review
- EZH2 inhibition enhances the activity of Carboplatin in aggressive-variant prostate cancer cell lines.Epigenomics · 2025Article
- New Insights into Potential Therapeutic Targets for Neuroendocrine Prostate Cancer: From Bench to Clinic.Research (Washington, D.C.) · 2025Review
- ASCL1 regulates and cooperates with FOXA2 to drive terminal neuroendocrine phenotype in prostate cancer.JCI insight · 2024Article
- Systematic Multi-Omics Investigation of Androgen Receptor Driven Gene Expression and Epigenetics changes in Prostate Cancer.bioRxiv : the preprint server for biology · 2024Article
- DPYSL5 is highly expressed in treatment-induced neuroendocrine prostate cancer and promotes lineage plasticity via EZH2/PRC2.Communications biology · 2024Article
- Understanding the role of Pax5 in development of taxane-resistant neuroendocrine like prostate cancers.Research square · 2023Article
- Role of transcription factors and chromatin modifiers in driving lineage reprogramming in treatment-induced neuroendocrine prostate cancer.Frontiers in cell and developmental biology · 2023Review
- Article
- Single-cell transcriptional regulation and genetic evolution of neuroendocrine prostate cancer.iScience · 2022Article
- Elevated ASCL1 activity creates de novo regulatory elements associated with neuronal differentiation.BMC genomics · 2022Article
- Aggressive variants of prostate cancer: underlying mechanisms of neuroendocrine transdifferentiation.Journal of experimental & clinical cancer research : CR · 2022Review
- Transcription Factors as Novel Therapeutic Targets and Drivers of Prostate Cancer Progression.Frontiers in oncology · 2022Review
- Regulation of Neuroendocrine-like Differentiation in Prostate Cancer by Non-Coding RNAs.Non-coding RNA · 2021Review
- Delineating the Molecular Events Underlying Development of Prostate Cancer Variants with Neuroendocrine/Small Cell Carcinoma Characteristics.International journal of molecular sciences · 2021Review
- Single-cell ATAC and RNA sequencing reveal pre-existing and persistent cells associated with prostate cancer relapse.Nature communications · 2021Article
- Article
- Role of specialized composition of SWI/SNF complexes in prostate cancer lineage plasticity.Nature communications · 2020Article
- MicroRNAs in treatment-induced neuroendocrine differentiation in prostate cancer.Cancer drug resistance (Alhambra, Calif.) · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroendocrine prostate cancer (NEPC) is thought to arise as prostate adenocarcinoma cells transdifferentiate into neuroendocrine (NE) cells to escape potent anti-androgen therapies however, the exact molecular events accompanying NE transdifferentiation and their plasticity remain poorly defined. Cell fate regulator ASCL1/hASH1's expression was markedly induced in androgen deprived (AD) LNCaP cells and prominent nuclear localisation accompanied acquisition of the NE-like morphology and expression of NE markers (NSE). By contrast, androgen-insensitive PC3 and DU145 cells displayed clear nuclear hASH1 localisation under control conditions that was unchanged by AD, suggesting AR signalling negatively regulated hASH1 expression and localisation. Synthetic androgen (R1881) prevented NE transdifferentiation of AD LNCaP cells and markedly suppressed expression of key regulators of lineage commitment and neurogenesis (REST and ASCL1/hASH1). Post-AD, NE LNCaP cells rapidly lost NE-like morphology following R1881 treatment, yet ASCL1/hASH1 expression was resistant to R1881 treatment and hASH1 nuclear localisation remained evident in apparently dedifferentiated LNCaP cells. Consequently, NE cells may not fully revert to an epithelial state and retain key NE-like features, suggesting a "hybrid" phenotype. This could fuel greater NE transdifferentiation, therapeutic resistance and NEPC evolution upon subsequent androgen deprivation. Such knowledge could facilitate CRPC tumour stratification and identify targets for more effective NEPC management.
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