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Cytotoxic Efficacy of Photodynamic Therapy in Osteosarcoma Cells In Vitro
Published on: March 18, 2014
Deoxyelephantopin Induces Reactive Oxygen Species-Mediated Apoptosis and Autophagy in Human Osteosarcoma Cells
Jilong Zou1, Yan Zhang1, Jiabing Sun1
1Department of Orthopaedics, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Background/Aims:
Osteosarcoma is the predominant form of primary bone malignancy. Although the combinational application of neoadjuvant chemotherapy and surgical resection significantly increases the survival rate, the therapeutic outcome remains unsatisfactory. Deoxyelephantopin (DET), an active ingredient of Elephantopus scaber, has been reported to have an anti-tumor effect in recent publications. This study aimed to investigate whether DET has antineoplastic effects on osteosarcoma cells and its underlying mechanism.
Methods:
Cell viability and morphological changes were assessed by MTT and Live/dead assays. Cell apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential were detected utilizing Annexin V-FITC/PI double staining, DCFH-DA and JC-1 probes, respectively. Autophagy was detected by mRFP-GFP-LC3 adenovirus transfection and western blot.
Results:
DET dose-dependently reduced the viability of osteosarcoma cells following the increase in intracellular ROS levels. Pretreatment with N-acetylcysteine (NAC) reversed this effect. Furthermore, DET induced mitochondrial apoptosis. Depolarized cells were increased, and apoptosis-related proteins, such as Bax, Bcl-2, cleaved caspase-9, cleaved caspase-3 and cleaved ploy ADP-ribose polymerase, were activated. Additionally, we found that DET could induce autophagy in osteosarcoma cells, but autophagy inhibition did not affect the decrease in cell viability.
Conclusion:
DET induced apoptosis in osteosarcoma cells through ROS generation, mitochondrial dysfunction and caspase activation; in addition, autophagy was involved in the effects of DET on osteosarcoma cells.
Insights
Deoxyelephantopin (DET) effectively reduces osteosarcoma cell viability by inducing apoptosis via reactive oxygen species (ROS) generation and mitochondrial dysfunction. Autophagy also plays a role in DET
Area of Science:
- Oncology
- Pharmacology
- Cell Biology
Background:
- Osteosarcoma is a primary bone cancer with unsatisfactory therapeutic outcomes despite current treatments.
- Deoxyelephantopin (DET), from Elephantopus scaber, shows potential anti-tumor properties.
Purpose of the Study:
- To investigate the antineoplastic effects of DET on osteosarcoma cells.
- To elucidate the underlying molecular mechanisms of DET's action.
Main Methods:
- Assessed cell viability (MTT) and morphology (Live/dead assays).
- Detected reactive oxygen species (ROS), mitochondrial membrane potential, and apoptosis (Annexin V-FITC/PI).
- Investigated autophagy using mRFP-GFP-LC3 transfection and western blot.
Main Results:
- DET reduced osteosarcoma cell viability in a dose-dependent manner, increasing intracellular ROS.
- DET induced mitochondrial apoptosis, evidenced by increased depolarization and activation of apoptosis-related proteins (Bax, Bcl-2, caspases).
- DET triggered autophagy in osteosarcoma cells, though autophagy inhibition did not alter cell viability reduction.
Conclusions:
- DET induces osteosarcoma cell apoptosis through ROS generation, mitochondrial dysfunction, and caspase activation.
- Autophagy is implicated in the anti-cancer effects of DET on osteosarcoma cells.
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