Lee KH, et al. - Researchers identified the histone demethylase KDM7A (which demethylates histone H3K27) as being overexpressed in enzalutamide resistant castration-resistant prostate cancer cell line C4-2b, so they looked for the molecular mechanism whereby androgen receptor activity is regulated by KDM7A. Following hormone stimulation in chromatin-immunoprecipitation experiments, KDM7A binding on androgen receptor target-gene promoters was corroborated. In KDM7A knock-down LNCaP stable cell, increased H3K27 di-methylation was observed. Reduced proliferation and apoptosis of prostate cancer cells were observed as the impacts of treatment with KDM7A inhibitor, TC-E 5002. A significant upregulation of the KDM7A protein in prostate cancer tissue was observed, and this difference showed correlation with the Gleason score. KDM7A was suggested to possibly be a good therapeutic target for prostate cancer drugs and could possibly be used as a good prognostic indicator for prostate cancer and associated strategies for treatment.