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Updated: Sep 28, 2025

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

Yang Yu1, Periyannan Velu2, Yulong Ma3

  • 1Department of Traumatic Joint Surgery, 3201 Hospital, Hanzhong, China.

Environmental Toxicology
|March 31, 2022
PubMed

Insights

Nerolidol effectively inhibited osteosarcoma cell growth by inducing oxidative stress and apoptosis. This natural compound also caused cell cycle arrest, showing potential as a bone cancer therapeutic.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • Osteosarcoma is a primary bone cancer with limited treatment options.
  • Natural compounds are being investigated for their anti-cancer properties.

Purpose of the Study:

  • To investigate the effects of nerolidol on osteosarcoma MG-63 cells.
  • To analyze cell proliferation, apoptosis, and cell cycle arrest mechanisms induced by nerolidol.

Main Methods:

  • Osteosarcoma MG-63 cells were treated with nerolidol (15 and 20 μM/ml).
  • Assays included MTT for proliferation, DCFH-DA for ROS, Rh-123 for mitochondrial potential, AO/EtBr, PI, DAPI staining for apoptosis, and Western blot/RT-PCR for protein/mRNA expression.
  • Cell cycle analysis was performed using flow cytometry.

Main Results:

  • Nerolidol significantly suppressed osteosarcoma cell proliferation in a dose-dependent manner.
  • Nerolidol induced oxidative stress, altered mitochondrial potential, and triggered apoptotic morphological changes.
  • Nerolidol regulated apoptosis-related proteins (Bax, Bcl-2) and kinases (ERK, P38, JNK) and arrested cells in the G0/G1 phase via the PI3K/AKT pathway.

Conclusions:

  • Nerolidol exhibits potent anti-cancer effects against osteosarcoma cells.
  • Nerolidol acts through induction of oxidative stress, apoptosis, and cell cycle arrest.
  • Nerolidol shows promise as a potential chemotherapeutic agent for bone cancer.
Keywords:
FACScanbone cancercell deathcell viabilitynerolidol

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