Crosstalk between EZH2 and DNA methylation mediates neuroendocrine prostate cancer lineage plasticity - PubMed
2 days ago
- #neuroendocrine
- #epigenetics
- #prostate cancer
- Prostate cancer lineage plasticity involves changes in DNA methylation and EZH2 activity.
- Hypomethylated DNA regions accumulate the repressive mark H3K27me3 in neuroendocrine prostate cancer (NEPC).
- EZH2 deletion or inhibition in NEPC models leads to genome-wide DNA methylation rewiring, affecting neuroendocrine-lineage genes.
- DNMT1 deletion alters H3K27me3 distribution, particularly at bivalent promoters with both H3K27me3 and H3K4me3 marks.
- In NEPC models, DNMT1 deletion increases H3K27me3 and represses neuroendocrine-lineage genes.
- In prostate adenocarcinoma models, DNMT1 deletion reduces H3K27me3 and de-represses neuroendocrine-lineage genes.
- The study reveals a functional interplay between EZH2 and DNA methylation in mediating prostate cancer lineage plasticity.