Calyxin Y has been recently isolated from Alpinia katsumadai which has a folk use as an anti-tumor medicine. Calyxin Y induced caspase-dependent cell death in NCI-H460 cells, and concomitantly, provoked cytoprotective autophagy with the upregulation of critical Atg proteins. The cleavage of Atg proteins by caspases acted as a switch between autophagy and apoptosis induced by calyxin Y. Intracellular hydrogen peroxide (H2O2) production was triggered upon exposure to calyxin Y via the induction of autophagy and apoptosis. We provided evidence that activated JNK was upstream effectors controlling both autophagy and apoptosis in response to elevated H2O2. Therefore, our findings demonstrate that calyxin Y serves multiple roles as a promising chemotherapeutic agent that induces H2O2-dependent autophagy and apoptosis via JNK activation.
Keywords: 2′,7′-dichlorofluorescein-diacetate; Apoptosis; Atg; Atgs; Autophagy; BCA; BSA; Calyxin Y; DCF; DCFH-DA; ECL; ERK; JNK; LC3; MAPK; PI; ROS; SDS–PAGE; TBST; autophagy related genes; bicinchoninic acid; c-Jun N-terminal protein kinases; dichlorofluorescein; enhanced chemiluminescence; extracellular signal-regulated kinases; fetal bovine serum albumin; microtubule-associated protein1 light chain 3; mitogen-activated protein kinase; propidium iodide; reactive oxygen species; sodium dodecyl sulfate–polyacrylamide gel electrophoresis; tris-buffered saline containing 0.1% Tween-20.
Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.