DIABETES & PANCREATITIS p85a Deficiency Protects ß-Cells from Endoplasmic Reticulum Stress-Induced Apoptosis Researchers demonstrated that reducing p85a expression in ß-cells can markedly delay the onset and severity of the diabetic phenotype observed in Akita+/- mice, which express a mutant insulin molecule. [Proc Natl Acad Sci USA] Abstract Lysine Deacetylase Inhibition Prevents Diabetes by Chromatin-Independent Immunoregulation and ß-Cell Protection Scientists demonstrated that the clinically well-tolerated KDACi vorinostat and givinostat revert diabetes in the nonobese diabetic mouse model of type 1 diabetes and counteract inflammatory target cell damage by a mechanism of action consistent with transcription factor-rather than global chromatin-hyperacetylation. [Proc Natl Acad Sci USA] Abstract Deoxysphingolipids, A Novel Biomarker for Type 2 Diabetes, Are Cytotoxic for Insulin-Producing Cells Researchers analyzed whether deoxysphingolipids directly compromise the functionality of insulin-producing Ins-1 cells and primary islets. Treatment with 1-deoxysphinganine induced dose-dependent cytotoxicity with senescent, necrotic and apoptotic characteristics and compromised glucose-stimulated insulin secretion. [Diabetes] Abstract IG20/MADD Plays a Critical Role in Glucose-Induced Insulin Secretion To investigate the role of IG20/MADD in ß-cell function researchers generated conditional knockout (KMA1ko) mice. KMA1ko ß-cells were able to process insulin normally, but had increased insulin accumulation and showed a severe defect in glucose-induced insulin release. [Diabetes] Abstract | Press Release PANCREATIC CANCER Loss of Canonical Smad4 Signaling Promotes KRAS Driven Malignant Transformation of Human Pancreatic Duct Epithelial Cells and Metastasis Investigators report that Smad4 represents a barrier in KRAS-mediated malignant transformation of the near normal immortalized human pancreatic duct epithelial cell line model. [PLoS One] Full Article The MEK/ERK Pathway Promotes NOTCH Signaling in Pancreatic Cancer Cells In pancreatic cancer cells, pulse of NOTCH1 activation led to increased expression of NOTCH target genes namely HES1 and c-MYC. Researchers uncovered that, upon its release, the NOTCH1 intracellular domain, NOTCH intracellular domain 1, undergoes a series of post-translational modifications that include phosphorylation. [PLoS One] Full Article CUB-Domain Containing Protein 1 Represses the Epithelial Phenotype of Pancreatic Cancer Cells To clarify the role of CUB-domain containing protein-1 (CDCP1) in pancreatic cancer, researchers examined the effects of CDCP1 knockdown on the cell behaviors of pancreatic cancer cells. Knockdown of CDCP1 expression in Panc-1 resulted in reduced cellular migration accompanied by the increased expression of E-cadherin and decreased expression of N-cadherin. [Exp Cell Res] Abstract Different Responses of Human Pancreatic Adenocarcinoma Cell Lines to Oncolytic Newcastle Disease Virus Infection In an effort to develop oncolytic virotherapy with Newcastle disease virus (NDV) for patients with pancreatic cancer, scientists evaluated the responses to NDV infection and interferon treatment of 11 different established human pancreatic adenocarcinoma cell lines (HPACs). Here they showed that all HPACs were susceptible to NDV. [Cancer Gene Ther] Abstract Overexpression of B7-H1 Correlates with Malignant Cell Proliferation in Pancreatic Cancer Researchers investigated the possible role of B7-H1 in the proliferation of pancreatic ductal adenocarcinoma (PDA) cells. Functional studies were performed using pancreatic cell lines that were genetically engineered to express high or low levels of B7-H1, and they found that the overexpression of B7-H1 through plasmid transfection in PDA cells promoted cell proliferation. [Oncol Rep] Abstract |