Functional characterization reveals PROX1 promotes tumor growth and metastasis in neuroendocrine prostate cancer, highlighting its potential as a therapeutic target.
Key Points
Knockout of prox1 inhibited tumor growth in neuroendocrine prostate cancer models, and overexpression increased metastasis.
CRISPR screening indicated high cellular dependency on prox1, crucial for maintaining aggressive NEPC characteristics.
Analysis revealed prox1's engagement in regulating neuroendocrine-lineage transcriptional programs across prostate cancer types.
Targeting prox1 phosphorylation via inhibitors may serve as a novel therapeutic strategy in combating NEPC.
Cite This Study
Venkadakrishnan et al. (2025) studied this question.