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Updated: Oct 6, 2025

Preparation of Naringenin Solution for In Vivo Application
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Preparation of Naringenin Solution for In Vivo Application

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Naringenin Induces ROS-Mediated ER Stress, Autophagy, and Apoptosis in Human Osteosarcoma Cell Lines

Chiang-Wen Lee1,2,3, Cathy Chia-Yu Huang4, Miao-Ching Chi5

  • 1Department of Nursing, Division of Basic Medical Sciences, Chronic Diseases and Health Promotion Research Center and Research Center for Chinese Herbal Medicine, Chang Gung University of Science and Technology, Puzi City 61363, Taiwan.

Molecules (Basel, Switzerland)
|January 21, 2022
PubMed

Insights

Naringenin effectively inhibits osteosarcoma cell growth by inducing apoptosis, cell cycle arrest, and autophagy. This natural compound shows promise as an alternative treatment for osteosarcoma by targeting key cellular pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Osteosarcoma is a primary bone tumor with poor response to conventional therapies.
  • There is a need for alternative treatments for osteosarcoma, especially in pediatric and young adult populations.
  • Naringenin, a natural flavonoid, has potential therapeutic properties.

Purpose of the Study:

  • To investigate the cytotoxic and antiproliferative effects of naringenin on osteosarcoma cell lines (HOS and U2OS).
  • To elucidate the underlying molecular mechanisms of naringenin's action, including apoptosis, cell cycle regulation, and autophagy.
  • To evaluate naringenin's impact on reactive oxygen species (ROS) generation, mitochondrial function, and endoplasmic reticulum (ER) stress.

Main Methods:

  • Cell viability and proliferation assessed using cell counting kit-8 and colony formation assays.
  • Apoptosis and cell cycle analysis performed via TUNEL assay, Annexin V/PI staining, and flow cytometry.
  • ROS generation, mitochondrial membrane potential, intracellular calcium levels, and protein expression (caspases, autophagy markers, cell cycle regulators) analyzed using flow cytometry and western blotting.

Main Results:

  • Naringenin significantly inhibited osteosarcoma cell viability and proliferation in a dose-dependent manner.
  • Naringenin induced G2/M cell cycle arrest by modulating cyclin B1, CDK1, and p21 expression.
  • Naringenin triggered apoptosis via ER stress, increased ROS production, and induced autophagy, leading to mitochondrial dysfunction.

Conclusions:

  • Naringenin exhibits significant antiproliferative effects on osteosarcoma cells.
  • Naringenin's mechanism involves the induction of apoptosis, cell cycle arrest, and autophagy through ROS production, mitochondrial dysfunction, and ER stress.
  • Naringenin represents a potential therapeutic agent for osteosarcoma treatment.
Keywords:
ER stressROSapoptosisautophagynaringeninosteosarcoma

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