Pterostilbene, a naturally occurring structural analog of resveratrol, has been 
reported to exert antiproliferative and proapoptotic effects in various cancer 
types. Recently, it has been demonstrated to induce both autophagy and apoptosis 
in human bladder and breast cancer cell lines. The aim of this study was to 
evaluate the effects of pterostilbene on HL60 human leukemia cells. Cell 
morphology was examined using confocal and electron microscopy. Cell viability 
was determined by MTT, neutral red uptake and trypan blue exclusion assays. LC3 
processing was studied based on Western blotting and immunofluorescence 
analyses. Flow cytometry was used to study cell cycle distribution, 
phosphatidylserine externalization, caspase activation, disruption of 
mitochondrial membrane potential and intracellular production of reactive oxygen 
species. DNA degradation was examined by gel electrophoresis. We found that 
treatment of HL60 cells with pterostilbene at the IC90 concentration resulted in 
the G0/G1 cell cycle arrest. Pterostilbene induced conversion of cytosolic LC3-I 
to membrane-bound LC3-II and accumulation of large LC3-positive vacuolar 
structures. Pterostilbene also led to phosphatidylserine externalization, 
internucleosomal DNA fragmentation, caspase activation and disruption of 
mitochondrial membrane potential. Moreover, it did not induce oxidative stress. 
Our results suggest that pterostilbene induces accumulation of autophagic 
vacuoles followed by cell death in HL60 cells.