LABORATORY RESEARCH Inhibition of Plk1 Represses Androgen Signaling Pathway in Castration-Resistant Prostate Cancer Scientists assessed the effects of polo-like kinase 1 (Plk1) on androgen receptor (AR) signaling in both androgen-dependent and androgen-independent prostate cancer cells. They demonstrated that the expression level of Plk1 correlated with tumorigenicity and that inhibition of Plk1 caused reduction of AR expression and AR activity. [Cell Cycle] Abstract Resveratrol Activates Autophagic Cell Death in Prostate Cancer Cells via Downregulation of STIM1 and the mTOR Pathway Investigators showed that resveratrol (RSV) activated autophagic cell death in PC3 and DU145 cells, which was dependent on stromal interaction molecule 1 (STIM1) expression. RSV treatment decreased STIM1 expression in a time-dependent manner and attenuated STIM1 association with TRPC1 and Orai1. [Mol Carcinog] Full Article Adipocyte-Derived Monocyte Chemotactic Protein-1 (MCP-1) Promotes Prostate Cancer Progression through the Induction of MMP-2 Activity Scientists investigated the biological role of MCP-1 secreted from adipocytes for prostate cancer cells. To characterize the physiological function of MCP-1 in the conditioned medium, they performed an MTT-assay, a wound-healing and invasion assay with anti-MCP-1 antibody using three prostate cancer cell lines: DU145, LNCaP, and PC-3. [Prostate] Abstract Metformin Represses Androgen-Dependent and Androgen-Independent Prostate Cancers by Targeting Androgen Receptor Metformin treatment reduced cell viability and enhanced apoptosis for the androgen-dependent LNCaP and the androgen-independent 22RV1 cell lines and additive effects were observed when LNCaP cells were treated with combined metformin and bicalutamide. Metformin down-regulated full-length androgen receptor protein in LNCaP cells. [Prostate] Abstract MicroRNA-302a Suppresses Tumor Cell Proliferation by Inhibiting AKT in Prostate Cancer The authors investigated the role of microRNA (miRNA)-302a in prostate cancer (PCa). Cell proliferation and cell cycle analysis were performed on PCa cells that stably expressed miRNA-302a. [PLoS One] Full Article mLST8 Promotes mTOR-Mediated Tumor Progression Knockdown of mLST8 significantly suppressed mTORC1 and mTORC2 complex formation, and it also inhibited tumor growth and invasiveness in human colon carcinoma and prostate cancer cells. [PLoS One] Full Article Increased Acid Ceramidase Expression depends on Upregulation of Androgen-Dependent Deubiquitinases, USP2, in a Human Prostate Cancer Cell Line, LNCaP USP2 siRNA decreased acid ceramidase (ACDase protein), while USP2 overexpression increased ACDase protein of LNCaP cells. However, SKP2, an ubiquitin E3 ligase, known to be active in prostate cancer, did not affect androgen-dependent ACDase expression in LNCaP cells. [J Biochem] Abstract Docetaxel in Combination with Octreotide Shows Synergistic Apoptotic Effect by Increasing SSTR2 and SSTR5 Expression Levels in Prostate and Breast Cancer Cell Lines Researchers investigated the possible synergistic apoptotic effects of docetaxel in combination with octreotide in prostate and breast cancer cell lines. [Cancer Chemother Pharmacol] Abstract CLINICAL RESEARCH A Randomized Phase II Trial of Sipuleucel-T with Concurrent vs Sequential Abiraterone Acetate plus Prednisone in Metastatic Castration Resistant Prostate Cancer This Phase II open-label study evaluated the effect of concurrent or sequential administration of abiraterone acetate plus prednisone on sipuleucel-T manufacture and immune responses in metastatic castration-resistant prostate cancer patients. [Clin Cancer Res] Abstract | Full Article AZD3514, an Oral Selective Androgen Receptor Down-Regulator in Patients with Castration-Resistant Prostate Cancer – Results of Two Parallel First-In-Human Phase I Studies In study 1 and 2, castration-resistant prostate cancer patients were initially recruited into a once daily oral schedule. In study 1, pharmacokinetic assessments led to twice daily dosing to increase exposure. Study 2 explored a once daily schedule. [Invest New Drugs] Abstract |