Inhibiting KDELC1 may prevent palmitate-induced apoptosis in INS-1 cells by reducing ER stress

Several endoplasmic reticulum resident proteins contain a unique C-terminal sequence Lys-Asp-Glu-Leu-KDEL, which is required for the retention of these proteins in the endoplasmic reticulum. Recently, the induction of endoplasmic reticulum (ER) stress is one mechanism proposed to contribute to the detrimental effects of FFA on beta-cells. In this study, INS-1 cells were exposed to PA and BSA for 24 hours. Cell viability was assessed using the Cell Counting Kit-8 (CCK8) viability assay. We use siRNA transfection method to inhibit the expression of KDELC1. The ER stress-related effectors were measured by western blotting. The results showed that the expression of ER stress-related chaperones GRP78, IRE1 alpha, ATF4 and Caspase-3 were reduced markedly after KDELC1 siRNA transfected in PA-induced INS-1 cells. And after silencing the expression of KDELC1, the cell viability was increased significantly. These finding provide that, inhibiting KDELC1 could reduce the expression of some ER stress-related chaperones and show a novel role for reduction of KDELC1 in preventing or treating with PA-treated insulinoma cell line.