LABORATORY RESEARCH Myeloid-Specific Expression of Ron Receptor Kinase Promotes Prostate Tumor Growth Researchers showed that the Ron receptor is expressed in mouse and human stromal cells of the prostate tumor microenvironment. To test the significance of stromal Ron expression, prostate cancer cells were orthotopically implanted into the prostates of either wild type or Ron tyrosine kinase deficient hosts. [Cancer Res] Abstract HIC1 Modulates Prostate Cancer Progression by Epigenetic Modification The methylation status of the HIC1 promoter were assayed in cell lines, tissues and plasma of prostate cancer patients by using MSP-PCR and bisulfate sequencing. The ability of HIC1 to regulate proliferation, migration and invasion was assessed by MTT, scratch healing assay and reconstituted extracellular matrices in porous culture chambers. [Clin Cancer Res] Abstract MicroRNA-182 and MicroRNA-200a Control G-Protein Subunit Alpha-13 (GNA13) Expression and Cell Invasion Synergistically in Prostate Cancer Cells G-protein coupled receptors signal through heterotrimeric G proteins, and among the different types of G proteins, GNA12/13 have been most closely linked to tumor progression. Investigators explored the role of GNA13 in prostate cancer cell invasion and the mechanism of up-regulation of GNA13 in these cells. [J Biol Chem] Abstract Targeting Constitutively Activated β1 Integrin Inhibits Prostate Cancer Metastasis By immunohistochemistry of human tissues, scientists found that levels of β1 integrins and integrin-induced autophosphorylation of FAK are increased in prostate cancer (PCa) cells in primary PCa and lymph node metastases, suggesting that β1 integrin activation occurs in metastatic progression of PCa. [Mol Cancer Res] Abstract A Feedback Regulation between Kindlin-2 and GLI1 in Prostate Cancer Cells The authors found that Kindlin-2 promotes GLI1 expression through a mechanism involving GSK3β inactivation and is independent of Smoothened. Functionally, knockdown of Kindlin-2 cooperates with cyclopamine, a Smoothened antagonist, to decrease the viability of prostate cancer cells. [FEBS Lett] Abstract Prostate Cancer Cells Metabolize D-Lactate inside Mitochondria via a D-Lactate Dehydrogenase which Is More Active and Highly Expressed than in Normal Cells Although D-lactate metabolism has been shown to occur in a variety of mitochondria, the metabolic fate of D-lactate in cancer cells has never been investigated, as it is believed to be exported to the extracellular phase. Scientists showed that mitochondria from both cancer and normal prostate cells can metabolize D-lactate in an energy competent manner. [FEBS Lett] Abstract A Novel Canine Model for Prostate Cancer Researchers sought to develop a canine model of prostate cancer that would more fully represent the features of human prostate cancer than existing models. [Prostate] Abstract CLINICAL RESEARCH Repurposing Itraconazole as a Treatment for Advanced Prostate Cancer: A Noncomparative Randomized Phase II Trial in Men With Metastatic Castration-Resistant Prostate Cancer Researchers conducted a noncomparative, randomized, Phase II study evaluating the antitumor efficacy of two doses of oral itraconazole in men with metastatic prostate cancer. [Oncologist] Abstract High-Grade Prostate Cancer and Biochemical Recurrence after Radical Prostatectomy among Men Using 5α-Reductase Inhibitors and Alpha-Blockers Two clinical trials have shown that users of 5α-reductase inhibitors finasteride and dutasteride (5-ARIs) have reduced overall prostate cancer risk, while the proportion of high-grade tumors is increased. The authors studied tumor characteristics, risk of biochemical recurrence and mortality after radical prostatectomy in 5-ARI and alpha-blocker users. [Prostate] Abstract |