Prostate Cell News Volume 6.38 | Oct 9 2015

MicroRNA-212 Negatively Regulates Starvation Induced Autophagy in Prostate Cancer Cells by Inhibiting SIRT1 and Is a Modulator of Angiogenesis and Cellular Senescence
Researchers demonstrated that microRNA (miR)-212 negatively modulates starvation induced autophagy in prostate cancer cells by targeting sirtuin 1 (SIRT1). Overexpression of miR-212 also leads to inhibition of angiogenesis and cellular senescence. [Oncotarget] Full Article

Co-Targeting Polo-Like Kinase 1 (Plk1) and the Wnt/β-Catenin Signaling Pathway in Castration-Resistant Prostate Cancer
Scientists showed that Plk1 is a negative regulator of Wnt/β-catenin signaling. Plk1 inhibition or depletion enhances the level of cytosolic and nuclear β-catenin in human prostate cancer cells. [Mol Cell Biol] Abstract

Differential Redox Regulation of Ca²⁺ Signaling and Viability in Normal and Malignant Prostate Cells
Researchers investigated alterations of intracellular Ca²⁺ and inhibition of cell viability caused by reactive oxygen species in primary human prostate epithelial cells (hPECs) from healthy tissue and prostate cancer cell lines. In hPECs, LNCaP and DU145 H₂O₂ induces an initial Ca²⁺ increase, which in prostate cancer cells is blocked at high concentrations of H₂O₂. [Biophys J] Abstract

GSK-3β Controls Autophagy by Modulating LKB1-AMPK Pathway in Prostate Cancer Cells
Inhibition of glycogen synthase kinase 3β (GSK-3β) activity resulted in a significant decline of cellular ATP production, leading to a significant increase of AMP/ATP ratio, a strong trigger of AMP-activated protein kinase (AMPK) activation in prostate cancer PC-3 cells. [Prostate] Abstract

The Influence of Prostatic Anatomy and Neurotrophins on Basal Prostate Epithelial Progenitor Cells
The effect of neurotrophins NGF, NT3, and BDNF were evaluated with respect to their influence on proliferation and activation of human basal prostate epithelial progenitor cells in vitro. [Prostate] Abstract

Combined Treatment with Exendin-4 and Metformin Attenuates Prostate Cancer Growth
Scientists examined the anti-cancer effect of Exendin–4 and metformin using a prostate cancer model. Exendin–4 and metformin additively decreased the growth curve, but not the migration, of prostate cancer cells. [PLoS One] Full Article

Anti-IL-20 Monoclonal Antibody Suppresses Prostate Cancer Growth and Bone Osteolysis in Murine Models
Researchers hypothesized that interleukin (IL)–20 promotes the growth of prostate cancer cells. In vitro, IL–20 upregulated N-cadherin, STAT3, vimentin, fibronectin, RANKL, cathepsin G, and cathepsin K, and increased the migration and colony formation of prostate cancer cells via activated p38, ERK1/2, AKT, and NF-κB signals in PC–3 cells. [PLoS One] Full Article

Antitumor Activity of Garcinol in Human Prostate Cancer Cells and Xenograft Mice
Garcinol, a polyisoprenylated benzophenone from fruits rinds of Garcinia indica, was studied for its antitumor activity by inducing apoptosis and inhibiting autophagy in human prostate cancer cells. The Bax/Bcl-2 ratio increased when garcinol was applied to PC-3 cells indicating a presence of apoptosis. [J Agric Food Chem] Abstract

CLINICAL RESEARCH

Haptoglobin Promoter Polymorphism rs5472 as a Prognostic Biomarker for Peptide Vaccine Efficacy in Castration-Resistant Prostate Cancer Patients
To detect a molecular prognosticator of clinical outcomes for personalized peptide vaccination (PPV), investigators analyzed whole-genome gene expression profiles of peripheral blood mononuclear cells in castration-resistant prostate cancer patients before administration of PPV. [Cancer Immunol Immunother] Abstract

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Oncolytics Biotech^® Inc. Announces Completion of Enrollment in Randomized Phase II Prostate Cancer Study
Oncolytics Biotech^® Inc. announced that enrollment has been completed in a randomized Phase II study of REOLYSIN^® in patients with recurrent or metastatic castration resistant prostate cancer. [Oncolytics Biotech^® Inc.] Press Release

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NEW PhD Studentships – Cancer Research (Cancer Research UK Manchester Institute)

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