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Updated: Apr 25, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
Published on: November 19, 2019
A therapeutic approach to treat prostate cancer by targeting Nm23-H1/h-Prune interaction
Marianeve Carotenuto1, Pasqualino de Antonellis, Cristina Maria Chiarolla
1Centro di Ingegneria Genetica e Biotecnologia Avanzate (CEINGE), Naples, Italy.
Abstract:
Nm23-H1 is a metastasis suppressor gene whose overexpression is associated with both reduced cell motility in various cancers and increased metastatic potential in neuroblastomas, osteosarcomas, and hematological malignances. We previously reported that Nm23-H1 exerts tumor suppressor action in prostate cancer cells and that h-Prune, which is overexpressed in various tumor types, binds Nm23-H1. Moreover, blockage of the Nm23-H1/h-Prune interaction with a competitive permeable peptide (CPP) attenuates migration of breast and neuroblastoma cells. This series of events suggests that the Nm23-H1/h-Prune protein complex regulates cancer progression and that its specific impairment could be a new therapeutic strategy in oncology. We found that CPP leads to inhibition of the AKT/mTORv and NF-kBv signaling pathways and also activates apoptosis. To obtain a proof-of-concept of our hypothesis, we used a xenograft model of prostate cancer to evaluate whether impairment of this complex using CPP results in an anti-tumoral effect. Using a mouse orthotopic model with bioluminescent imaging, we show evidences that CPP reduces prostate cancer metastases formation. In conclusion, CPP being able to impair formation of the h-Prune/Nm23-H1 complex holds promise for the treatment of prostate cancer.
Insights
A novel peptide (CPP) disrupts the Nm23-H1/h-Prune complex, inhibiting prostate cancer cell migration and reducing metastasis. This peptide shows promise as a new therapeutic strategy for prostate cancer treatment.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Metastasis Research
Background:
- Nm23-H1 acts as a metastasis suppressor gene, with its interaction with h-Prune influencing cancer progression.
- h-Prune is overexpressed in various tumors and binds Nm23-H1, suggesting a role in cancer.
- Previous studies indicate that blocking the Nm23-H1/h-Prune interaction with a competitive permeable peptide (CPP) reduces cancer cell migration.
Purpose of the Study:
- To investigate the anti-tumoral effect of impairing the Nm23-H1/h-Prune complex using CPP in a prostate cancer xenograft model.
- To evaluate CPP's potential as a therapeutic strategy for prostate cancer.
Main Methods:
- Utilized a mouse orthotopic xenograft model of prostate cancer.
- Employed bioluminescent imaging to track tumor progression and metastasis.
- Assessed the impact of CPP on AKT/mTOR and NF-kB signaling pathways and apoptosis.
Main Results:
- CPP significantly reduced prostate cancer metastasis formation in the xenograft model.
- CPP was shown to inhibit AKT/mTOR and NF-kB signaling pathways.
- CPP treatment also induced apoptosis in cancer cells.
Conclusions:
- Impairing the h-Prune/Nm23-H1 complex with CPP demonstrates anti-tumoral effects in prostate cancer.
- CPP holds promise as a potential therapeutic agent for treating prostate cancer by reducing metastasis.
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