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

Abstract

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.

Nerolidol inhibited U-251 human glioblastoma cell proliferation and triggered apoptosis via the upregulation of the p38 MAPK signaling pathway

“…Similar anti-proliferative and apoptotic properties of NRD were reported in hepatocellular carcinoma 27 and osteosarcoma. 28 Our findings demonstrate that NRD inhibited proliferation and stimulated apoptosis in U-251 cells.…”

“…propagation, incursion and metastasis, 16 and several phytochemicals act by inhibiting proliferation, invasion, metastasis, angiogenesis, and stimulating apoptosis. 14,15 The anticancer effects of NRD have been extensively explored in numerous cancers, including breast cancer, 22 hepatocellular carcinomas, 28 osteosarcomas, 29 oral cancer, 30 and ovarian cancer. 24 The current research evaluated the anti-GBM effects of NRD by assessing its anti-proliferative, cell-cycle protein regulation and apoptotic properties.…”

A novel Ni-based complex inducing apoptosis through mitochondrial dysfunction in osteosarcoma HOS cells

“…The formation of cancerous growths begins with a disturbance in the cell division process of cancer cells. 20 Several chemotherapeutic agents have been found to be crucial in causing cell cycle arrest at the G0/G1 phase. To comprehend the relationship between the Ni complex and growth inhibition and cell cycle arrest, we have examined the effects of the Ni complex on cell cycle progression.…”