Abstract
RESULTS: The WST assay revealed that the number of viable cells was reduced after NCL1 and NCD38 treatment. ChIP showed NCL1-induced H3K9me2 accumulation at the ELK4 and KLK2 promoters. Flow cytometry showed that NCL1 dose-dependently induced apoptosis. Using TEM analysis, autophagosomes were observed in LNCaP cells treated with NCL1. The combination index analysis further revealed that a combination of NCL1 and CQ significantly decreased cell growth synergistically. When NCL1 and NCD38-treated mice were compared with controls, the xenograft tumor volume was reduced with no adverse effects. CONCLUSIONS: Castration resistant prostate cancer growth was effectively suppressed with NCL1 and NCD38 both in vitro and in vivo without adverse events via regulation of apoptosis and autophagy, indicating the potential use of LSD1 inhibitors as therapeutic agents for prostate cancer.
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