LABORATORY RESEARCH N-Myc Drives Neuroendocrine Prostate Cancer Initiated from Human Prostate Epithelial Cells Scientists defined N-Myc and activated AKT1 as oncogenic components sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and neuroendocrine prostate cancer (NEPC) with phenotypic and molecular features of aggressive, late-stage human disease. They directly showed that prostate adenocarcinoma and NEPC can arise from a common epithelial clone. [Cancer Cell] Abstract | Graphical Abstract | Press Release PTP1B Deficiency Enables the Ability of a High Fat Diet to Drive the Invasive Character of PTEN-Deficient Prostate Cancers Scientists present genetic evidence in the mouse showing that prostate cancer progression driven by loss of the tumor suppressor Pten is mainly unresponsive to a high fat diet, but that coordinate loss of the protein tyrosine phosphatase Ptpn1 enables a highly invasive disease. [Cancer Res] Abstract Endogenous GAS6 and Mer Receptor Signaling Regulate Prostate Cancer Stem Cells in Bone Marrow The authors investigated the role that endogenous GAS6 and Mer receptor signaling plays in establishing prostate cancer stem cells in the bone marrow microenvironment. [Oncotarget] Full Article The Retinoblastoma Protein Regulates Hypoxia-Inducible Genetic Programs, Tumor Cell Invasiveness and Neuroendocrine Differentiation in Prostate Cancer Cells Investigators characterized the role retinoblastoma protein (Rb) plays in mediating hypoxia-regulated genetic programs by stably ablating Rb expression with retrovirally-introduced short hairpin RNA in LNCaP and 22Rv1 human prostate cancer cells. [Oncotarget] Full Article Activin A Regulates MicroRNAs and Gene Expression in LNCaP Cells No studies have investigated the impact of activin A on microRNA (miRNA) expression in prostate cancer (PCa) cell lines. Hence, the authors determined the effect of activin A on miRNA expression and downstream target genes in PCa. [Prostate] Abstract Epigenetics Reactivation of Nrf2 in Prostate TRAMP C1 Cells by Curcumin Analogue FN1 Researchers explored the epigenetic modification of FN1 that restores Nrf2 expression in TRAMP-C1 cells. Stably transfected HepG2-C8 cells were used to investigate the effect of FN1 on the Nrf2- antioxidant response element pathway. [Chem Res Toxicol] Abstract | Graphical Abstract A Triad of Telomerase, Androgen Receptor and Early Growth Response 1 in Prostate Cancer Cells Researchers demonstrated a decline in the hTERT expression and telomerase activity on “loss of AR” in androgen-dependent prostate cancer cells. They further addressed two unresolved queries, whether AR-mediated signaling is of any relevance to hTERT expression in castration-resistant prostate cancer and whether this signaling involves EGR1. [Cancer Biol Ther] Abstract MicroRNA-495 Regulates Migration and Invasion in Prostate Cancer Cells via Targeting Akt and mTOR Signaling Investigators identified a novel microRNA (miR)-495, which was downregulated in prostate cancer, but not normal prostate cell lines. MiR-495 directly targeted the 3′-UTR of Akt and mTOR mRNAs. [Cancer Invest] Abstract CLINICAL RESEARCH A Phase II Clinical Trial of Everolimus plus Bicalutamide for Castration-Resistant Prostate Cancer Patients who were eligible for this study had to have progressive castration-resistant prostate cancer with serum testosterone levels <50 ng/dL. No prior bicalutamide or everolimus was allowed. Treatment included oral bicalutamide 50 mg and oral everolimus 10 mg, both once daily, with a cycle defined as four weeks. [Cancer] Abstract Enzalutamide in Japanese Patients with Chemotherapy-Naïve, Metastatic Castration-Resistant Prostate Cancer: A Post-Hoc Analysis of the Placebo-Controlled PREVAIL Trial Asymptomatic or mildly symptomatic chemotherapy-naïve patients with metastatic castration-resistant prostate cancer progressing on androgen deprivation therapy were randomized one-to-one to 160 mg/day oral enzalutamide or placebo until discontinuation on radiographic progression or skeletal-related event and initiation of subsequent antineoplastic therapy. [Int J Urol] Abstract |