Androgen receptor (AR) suppresses DPYSL5, and overexpression of DPYSL5 promotes prostate cancer cell plasticity via EZH2-mediated PRC2 activation, suggesting that the AR/DPYSL5/EZH2/PRC2 axis may act as a driver of treatment-induced neuroendocrine prostate cancer.
- Roosa Kaarijärvi
- Heidi Kaljunen
- Kirsi Ketola