LABORATORY RESEARCH Efficacious Delivery of Protein Drugs to Prostate Cancer Cells by PSMA-Targeted pH-Responsive Chimaeric Polymersomes Scientists report that 2-[3-[5-amino-1-carboxypentyl]-ureido]-pentanedioic acid-decorated pH-responsive chimaeric polymersomes efficiently deliver therapeutic proteins into prostate cancer cells. The in vitro release results showed that protein release was markedly accelerated at mildly acidic pH due to the hydrolysis of acetal bonds in the vesicular membrane. [J Control Release] Abstract 3D Porous Chitosan-Alginate Scaffolds as an In Vitro Model for Evaluating Nanoparticle-Mediated Tumor Targeting and Gene Delivery to Prostate Cancer The authors investigated if prostate cancer cells cultured in three-dimensional (3D) chitosan-alginate porous scaffolds could model cationic nanoparticle-mediated gene targeted delivery to tumors in vitro. [Biomacromolecules] Abstract MicroRNA-195 Suppresses Tumor Cell Proliferation and Metastasis by Directly Targeting BCOX1 in Prostate Carcinoma Forced expression of miR-195 in prostate cancer (PCa) cells drastically inhibited proliferation, migration and invasion in vitro and inhibited tumor growth and metastasis in vivo. BCOX1 was identified as a direct target of miR-195 in PCa, and was found to be drastically increased in metastatic PCa [J Exp Clin Cancer Res] Full Article MicroRNA-195-5p, a New Regulator of Fra-1, Suppresses the Migration and Invasion of Prostate Cancer Cells MicroRNA (miR)-195 was frequently down-regulated in both prostate cancer cell lines, DU145 and PC3. Overexpression of miR-195 significantly repressed the capability of migration and invasion of prostate cancer cells. [J Transl Med] Full Article miR-378 Suppresses Prostate Cancer Cell Growth through Downregulation of MAPK1 In Vitro and In Vivo Researchers evaluated the anti-proliferative role of microRNA (miR)-378 in prostate cancer. They found that the expression of miR-378 was significantly downregulated in clinical prostate cancer tissues. In vitro assay suggested that overexpression of miR-378-suppressed prostate cancer cell migration and invasion promoted cell apoptosis. [Tumor Biol] Abstract The Bifunctional Autophagic Flux by 2-Deoxyglucose to Control Survival or Growth of Prostate Cancer Cells Rapamycin and LC3B overexpressing vectors were administered to prostate cancer cells (PC3) cells for autophagy induction and chloroquine and shBeclin1 plasmid were used to inhibit autophagy in PC3 cells to analyze PC3 cells growth and survival. [BMC Cancer] Full Article SILAC-Based Mass Spectrometry Analysis Reveals that Epibrassinolide Induces Apoptosis via Activating Endoplasmic Reticulum Stress in Prostate Cancer Cells The mechanism by which epibrassinolide exerts its effects on LNCaP is poorly understood. To address this gap in knowledge, researchers used an unbiased global proteomics approach, i.e., stable-isotope labeling by amino acids in cell culture (SILAC). [PLoS One] Full Article KML001 Induces Apoptosis and Autophagic Cell Death in Prostate Cancer Cells via Oxidative Stress Pathway The authors investigated the effects of KML001, an orally bioavailable arsenic compound, on the growth and death of human prostate cancer cells and its mechanism of action. [PLoS One] Full Article Cigarette Smoke Modulates PC3 Prostate Cancer Cell Migration by Altering Adhesion Molecules and the Extracellular Matrix The influence of cigarette smoke medium on cell migration and on the expression of extracellular matrix- and cell adhesion molecule-related genes in PC3 prostate adenocarcinoma cells was investigated. [Mol Med Rep] Abstract CLINICAL RESEARCH Safety of Long-Term Denosumab Therapy: Results from the Open Label Extension Phase of Two Phase III Studies in Patients with Metastatic Breast and Prostate Cancer Patients with metastatic breast or prostate cancer received subcutaneous denosumab 120 mg Q4W or intravenous zoledronic acid 4 mg Q4W in a double-blinded fashion. Denosumab demonstrated superior efficacy in the blinded treatment phase; thus, patients were offered open-label denosumab for up to an additional 2 years. [Support Care Cancer] Full Article |