This study finds that PROX1 promotes tumor growth in neuroendocrine prostate cancer, suggesting potential therapeutic targets through epigenetic derepression.
Key Points
Knockout of PROX1 impeded tumor growth in neuroendocrine prostate cancer models, highlighting its role as a cellular dependency.
CRISPR screens in NEPC organoid models revealed high cellular dependency on PROX1 for tumor growth and metastasis.
Mass spectrometry identified critical phosphorylated sites in the DNA-binding domain of PROX1, essential for its function and stability.
Inhibition of upstream kinases like CHEK1 and CDK2 reduced NEPC viability, indicating avenues for targeted treatment.
Cite This Study
Venkadakrishnan et al. (2025) studied this question.