Nerolidol induced apoptosis via PI3K/JNK regulation through cell cycle arrest in MG‐63 osteosarcoma cells

The aim of the present study was to determine the cell proliferation, apoptotic pathway analysis through protein, mRNA and cell cycle arrest mechanism in nerolidol induced osteosarcoma MG-63 cells. The osteosarcoma MG-63 cells were treated with various doses of nerolidol (15 and 20 μM/ml) for 24 h. Cell proliferation was examined using assist method of MTT assay, fixed the IC50 value of nerolidol 15 μM/ml. Reactive oxygen species (ROS) generation was analyzed by DCFH-DA dye, mitochondrial potential detected by Rh-123 dye, apoptotic morphological changes identified by AO/EtBr, PI, DAPI staining, and cell adhesion were detected by using fluorescence microscope. Cell proliferation, and apoptotic molecular protein and mRNA expressions such as ERK, P38, p-PI3K, p-JNK, Bcl-2, JNK, p-P38, cyclin-D1, and Bax were analyzed in osteosarcoma MG-63 cells. Nerolidol significantly suppressed the osteosarcoma cells progression in a dose dependent manner (p < .05) evident in the oxidative stress induction and apoptotic morphological changes. Nerolidol also regulated the protein PI3K/AKT mechanistically via induction of apoptosis Nerolidol suppresses osteosarcoma MG-63 cells by PI3K/AKT by cell cycle arrest at early phase of G0/G1. To sum up, nerolidol suppressed the growth of bone cancer cells and can be finally targeted as a potent drug for analyzing its chemotherapeutic effects in future.