ArticleCancer research2025
Epigenetic Derepression of PROX1 Promotes Neuroendocrine Prostate Cancer Progression.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Vitronectin Enrichment in Prostate Cancer Liver Metastases Promotes Adhesion and Survival.Cancer research communications · 2026Article
- Triptolide sensitizes cancer cells to nucleoside DNA methyltransferase inhibitors through inhibition of DCTPP1-mediated cell-intrinsic resistance.Nature communications · 2026Article
- Tumor-Associated Macrophage Exosomal miR-142-5p Drives Prostate Cancer Neuroendocrine Differentiation via RERG/Ras/ERK Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- 3D genome architecture and epigenetic regulation of lineage identity in advanced prostate cancer.Endocrinology · 2026Review
- NF-κB-driven lymphangiogenesis affects kidney function via a VEGFR-3-mediated pathway.JCI insight · 2026Article
- EZH2 Suppression Diversifies Prostate Cancer Lineage Variant Evolution and Lacks Efficacy in Inhibiting Disease Progression.Cancer research · 2026Article
- Senescence-related gene signature predicts prostate cancer progression and identifies PCNA as a therapeutic target via multi-omics machine learning integration.British journal of cancer · 2026Article
- Patient-derived prostate cancer organoids: model development, therapeutic applications, and challenges for precision oncology.Frontiers in oncology · 2026Review
- The Quartet of Core Oncogenic Drivers in Neuroendocrine Prostate Cancer: Multi-Omics Dataset Integration to Forge a Translational Link Between Biology and Precision Therapy.International journal of biological sciences · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Histologic transformation of prostate cancer from adenocarcinoma to neuroendocrine prostate cancer (NEPC) is associated with aggressive disease and poor prognosis. This lineage transition is accompanied by polycomb complex 2-mediated epigenetic derepression of cell fate-determining transcription factors, including prospero homeobox 1 (PROX1). In this study, we sought to functionally characterize the role of PROX1 in NEPC. An unbiased CRISPR screen in two NEPC patient-derived organoid models demonstrated high cellular dependency for PROX1. Knockout of PROX1 impeded tumor growth in NEPC models, and overexpression of PROX1 promoted tumor growth and spontaneous metastasis in prostate adenocarcinoma. Transcriptomic and cistromic analyses across castration-resistant adenocarcinoma and neuroendocrine models pointed to PROX1-mediated regulation of neuroendocrine-lineage transcriptional programs. Immunoprecipitation followed by mass spectrometry identified three phosphorylated sites in the DNA-binding domain of PROX1 that are critical for its stability and function. CHEK1 and CDK2 were predicted to be upstream kinases that phosphorylate PROX1, and treatment with a CHEK1 or CDK2 inhibitor reduced NEPC viability. Together, these results substantiate the role of PROX1 in NEPC and identify PROX1 phosphorylation in the DNA-binding domain, which might represent a therapeutic target in NEPC. SIGNIFICANCE: PROX1 mediates lineage reprogramming, tumor growth, and metastasis in neuroendocrine prostate cancer and represents a cellular dependency that can be exploited for targeted treatment strategies.
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Registered trials
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