DIABETES & PANCREATITIS Inhibition of Ca2+-Independent Phospholipase A2 (iPLA2β) Ameliorates Islet Infiltration and Incidence of Diabetes in NOD Mice Scientists assessed the effects of iPLA2β inhibition on diabetes development. Administration of FKGK18, a reversible iPLA2β inhibitor, to non-obese diabetic (NOD) mice significantly reduced diabetes incidence in association with reduced insulitis, reflected by reductions in CD4+ T-cells and B-cells, improved glucose homeostasis, higher circulating insulin, and β-cell preservation. [Diabetes] Abstract p21WAF1/Cip1 Limits Senescence and Acinar-to-Ductal Metaplasia Formation during Pancreatitis Scientists investigated whether p21 down-regulation is implicated in controlling the early events of acinar cell trans-differentiation and acinar-to-ductal metaplasia (ADM) formation. They found that p21 was strongly up-regulated in wild type acinar cells during pancreatitis while absent in ADM areas, suggesting that p21 down-regulation is associated with ADM formation. [J Pathol] Abstract Autocrine Activation of P2Y1 Receptors Couples Ca2+ Influx to Ca2+ Release in Human Pancreatic Beta Cells Investigators examined the effects of purinergic agonists and antagonists on membrane potential, membrane currents, intracellular Ca2+ and insulin secretion in human beta cells. [Diabetologia] Abstract Novel Role for Matricellular Proteins in the Regulation of Islet β Cell Survival: The Effect of SPARC on Survival, Proliferation and Signaling Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that is important for the regulation of cell growth and adhesion. Researchers investigated the role of SPARC in the regulation of β cell growth and survival. [J Biol Chem] Abstract | Full Article PANCREATIC CANCER Pancreatic Cancer-Specific Cell Death Induced In Vivo by Cytoplasmic-Delivered Polyinosine-Polycytidylic Acid Researchers investigated the potential therapeutic activity of a formulation of polyinosine-polycytidylic acid (pIC) with polyethylenimine ([pIC]PEI) in PDAC and investigated its mechanism of action. [pIC]PEI stimulated apoptosis in PDAC cells without affecting normal pancreatic epithelial cells. [Cancer Res] Abstract Glucagon-Like-Peptide-1 Receptor Expression in Normal and Diseased Human Thyroid and Pancreas 221 human thyroid and pancreas samples were analyzed for glucagon-like-peptide-1 receptor (GLP1R) immunohistochemistry and compared with quantitative in vitro GLP1R autoradiography. All ductal pancreatic carcinomas are GLP1R negative, whereas 6/20 PanIN 1/2 and 0/12 PanIN 3 express GLP1R. [Mod Pathol] Abstract Elongation Factor-2 Kinase Regulates TG2/β1 Integrin/Src/uPAR Pathway and Epithelial-Mesenchymal Transition Mediating Pancreatic Cancer Cell Invasion Researchers investigated the role of eukaryotic elongation factor-2 kinase (eEF-2K) in cellular invasion and found that down-regulation of eEF-2K by siRNA or rottlerin displays impairment of pancreatic cancer cell invasion/migration with significant decreases in the expression of tissue transglutaminase, the multifunctional enzyme implicated in regulation of cell attachment, motility and survival. [J Cell Mol Med] Full Article SUMO-Specific Protease 1 Regulates Pancreatic Cancer Cell Proliferation and Invasion by Targeting MMP-9 Investigators show that sentrin/SUMO-specific protease 1 (SENP1) was upregulated in pancreatic ductal adenocarcinoma (PDAC) tissues compared with adjacent normal tissues. Knockdown of SENP1 by SENP1-siRNA inhibited pancreatic cancer cell proliferation, migration, and invasion, suggesting that SENP1 plays an important role in PDAC progression and metastasis. [Tumor Biol] Abstract GRP78 Promotes the Invasion of Pancreatic Cancer Cells by FAK and JNK To investigate the effect of glucose-regulated protein 78 (Grp78) on the invasion of pancreatic cancer, researchers used western blot and Transwell assay. They found Grp78 is expressed at lower levels in capan-2 and higher expressed in MiaPaCa-2 cells, and Grp78 expression levels were correlated with the invasion potentials of tumor cells. [Mol Cell Biochem] Abstract |