glyx-13-peptide and Colorectal-Neoplasms

To investigate the effect of propofol on glucose metabolism in colorectal cancer cells and in an in vivo xenograft model.. Glucose metabolism was assessed by measuring the extracellular acidification rate in HT29 and SW480 colorectal cancer cells. Quantitative real-time PCR and western blot analyses were used to detect mRNA and protein levels, respectively. Intracellular calcium was assessed by using a Fluo-3 AM fluorescence kit. Micro-positron emission tomography/computed tomography (microPET/CT) imaging was used to analyze glucose metabolism in the tumors of the xenograft model.. Propofol exposure induced a dose-dependent decrease of aerobic glycolysis in HT29 and SW480 colorectal cancer cells. MicroPET/CT indicated that propofol also inhibited 18F-FDG uptake in the xenograft model. In addition, hypoxia-inducible factor 1α (HIF1α) was also reduced by propofol dose-dependently. Propofol repressed the NMDAR-CAMKII-ERK pathway to inactivate HIF1α and therefore reduced glycolysis.. Propofol inhibited aerobic glycolysis in colorectal cancer cells through the inactivation of the NMDAR-CAMKII-ERK pathway, which may facilitate a better understanding of the use of propofol in the clinical setting.

Topics: Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2; Cell Line, Tumor; Colorectal Neoplasms; Dizocilpine Maleate; Down-Regulation; Extracellular Signal-Regulated MAP Kinases; Female; Fluorodeoxyglucose F18; Glucose Transporter Type 1; Glycolysis; HT29 Cells; Human Umbilical Vein Endothelial Cells; Humans; Mice; Mice, Inbred BALB C; Oligopeptides; Phosphoglycerate Kinase; Prognosis; Propofol; Receptors, N-Methyl-D-Aspartate; Signal Transduction