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
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
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
REVIEWS
KRAS: Feeding Pancreatic Cancer Proliferation A number of studies have shown that oncogenic KRAS plays a central role in controlling tumor metabolism by orchestrating multiple metabolic changes including stimulation of glucose uptake, differential channeling of glucose intermediates, reprogrammed glutamine metabolism, increased autophagy, and macropinocytosis. The authors review these recent findings and address how they may be applied to develop new pancreatic ductal adenocarcinoma treatments. [Trends Biochem Sci] Abstract
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