Related Experiment Video
Updated: Mar 12, 2026
Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro
Published on: March 18, 2014
Parthenolide Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in Human Osteosarcoma Cells
Chen Yang1, Qing Ou Yang, Qing-Jie Kong
1Department of orthopedic Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, China.
Background And Aim:
Osteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Parthenolide, a naturally occurring small molecule that interferes with NF-κB signaling, has recently attracted considerable attention because of its pharmacological action involving anti-cancer effects. However, the mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today.
Methods:
In this study, the effects of parthenolide were evaluated and characterized in human osteosarcoma cancer cell. Cell viability was assessed by CCK-8. Apoptosis was assessed by Annexin V-FITC/PI Flow cytometry assay. Relative quantitative real-time PCR and western blot were used to determine the expressions of genes and proteins.
Results:
Our results suggest that parthenolide did not cause caspase-dependent cell death in osteosarcoma cancer cells, as indicated by the absence of significant early apoptosis as well as caspase-3 cleavage. Instead, parthenolide increased the autophagy and mitophagy, as characterized by increased PINK1 and Parkin translocation to mitochondria and enhanced autophagy proteins. The induction of autophagy by parthenolide was associated with the increase of reactive oxygen species (ROS). ROS antioxidants N-acetylcysteine (NAC) attenuated parthenolide-induced autophagy activity.
Conclusions:
Our findings unveil a novel mechanism of drug action by parthenolide in osteosarcoma cancer cells and suggest a potential value of treating osteosarcoma cancer through a caspase-independent autophagic cell death by ROS activation.
Insights
Parthenolide induces autophagy and mitophagy, not apoptosis, in osteosarcoma cells. This novel mechanism involves reactive oxygen species (ROS) and suggests potential for treating osteosarcoma via ROS-activated autophagic cell death.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Osteosarcoma is a primary bone tumor affecting adolescents.
- Parthenolide, a natural compound, exhibits anti-cancer effects by interfering with NF-κB signaling.
- The precise mechanism of parthenolide's cytotoxic action in tumor cells remains unclear.
Purpose of the Study:
- To investigate the mechanism of parthenolide's cytotoxic effect on human osteosarcoma cells.
- To characterize the cell death pathway induced by parthenolide.
Main Methods:
- Cell viability assessed using CCK-8 assay.
- Apoptosis evaluated via Annexin V-FITC/PI Flow cytometry.
- Gene and protein expression analyzed by real-time PCR and Western blot.
Main Results:
- Parthenolide did not induce caspase-dependent apoptosis or caspase-3 cleavage.
- Parthenolide significantly increased autophagy and mitophagy, evidenced by PINK1/Parkin translocation and enhanced autophagy proteins.
- Autophagy induction correlated with increased reactive oxygen species (ROS), which were attenuated by N-acetylcysteine (NAC).
Conclusions:
- Parthenolide triggers a novel caspase-independent autophagic cell death pathway in osteosarcoma.
- ROS activation plays a crucial role in parthenolide-induced autophagy.
- Parthenolide shows potential for osteosarcoma treatment through ROS-mediated autophagic cell death.
Related Concept Videos
01:18Autophagic Cell Death
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
01:30Overview of Cell Death
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...