Coactivator MYST1 Regulates Nuclear Factor-κB and Androgen Receptor Functions During Proliferation of Prostate Cancer Cells

摘要: In prostate cancer (PCa), the functional synergy between androgen receptor (AR) and nuclear factor-κ B (NF-κB) escalates resistance to therapeutic regimens promotes aggressive tumor growth. Although underlying mechanisms are less clear, gene regulatory abilities of coactivators can bridge transcription functions AR NF-κB. The present study shows that MYST1 (MOZ, YBF2 SAS2, TIP60 protein 1) costimulates NF-κB in PCa cells. We demonstrate activation deacetylation by sirtuin 1. Further, mutually exclusive interactions with 1 vs regulate acetylation lysine 16 on histone H4. Notably, AR-lacking PC3 cells AR-depleted LNCaP cells, diminution activates cleavage poly(ADP-ribose) polymerase caspase 3 leads apoptosis. contrast, AR-transformed (PC3-AR), depletion induces cyclin-dependent kinase (CDK) N1A/p21, which results G2M arrest. Concomit...