ArticleClinical cancer research : an official journal of the American Association for Cancer Research2025
Emerin Dysregulation Drives the Very-Small-Nuclear Phenotype and Lineage Plasticity That Associate with a Clinically Aggressive Subtype of Prostate Cancer.
Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Nuclear envelope proteins in cancer: revisiting the significance of LEM-domain proteins.Frontiers in cell and developmental biology · 2026Review
- TLN1 interacts with NGFR and suppresses the development of castration-resistant prostate cancer by upregulating NGFR.Frontiers in immunology · 2026Article
- In vivo self-assembled nano-PROTAC for the dual degradation of AR and HSP90 to overcome castration-resistant prostate cancer resistance.Signal transduction and targeted therapy · 2025Article
- Emerin expression stratification across breast cancer subtypes.Cancer treatment and research communications · 2025Article
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21 authors.
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Abstract
purposeCirculating tumor cells (CTC) with a very-small-nuclear phenotype (vsnCTC) in prostate cancer are characterized by nuclei smaller than 8.5 μm. Our previous studies established an association between vsnCTCs and visceral metastasis. Reduction of emerin (EMD), a nuclear envelope protein, contributes to prostate cancer metastasis and nuclear shape instability. In this study, we investigated the correlation between EMD expression and the vsnCTC phenotype and its clinical impact. EXPERIMENTAL
designWe analyzed CTCs from 93 patients with metastatic castration-resistant prostate cancer and categorized them as either vsnCTC+ or vsnCTC- and compared overall survival and progression-free survival. C4-2B, 22Rv1, and DU145 with EMD knockdown were developed and characterized by nuclear size and gene expression by gene set enrichment analysis. Abiraterone- and enzalutamide-resistant C4-2B cells were also characterized by nuclear size and EMD expression.
resultsPatients who were vsnCTC+ had significantly worse overall survival and progression-free survival compared with patients who were vsnCTC-. EMD expression was markedly reduced in CTCs from patients who were vsnCTC+ compared with patients who were vsnCTC-, with a significant positive correlation between EMD expression and CTC nuclear size. EMD knockdown in prostate cancer cells resulted in smaller nuclei, enhanced invasion, and the upregulation of genes associated with lineage plasticity. Additionally, abiraterone- and enzalutamide-resistant C4-2B cells had smaller nuclei and lower EMD expression. vsnCTC+ cells also showed enhanced platinum sensitivity.
conclusionsThe presence of vsnCTCs represents a novel hallmark of an aggressive subtype of metastatic castration-resistant prostate cancer closely linked to EMD loss and lineage plasticity. These findings highlight the importance of EMD dysregulation in the vsn phenotype, disease progression, and therapeutic resistance in patients with prostate cancer.
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