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Updated: Jun 12, 2025
Basic Research in Plasma Medicine - A Throughput Approach from Liquids to Cells
Published on: November 17, 2017
Non-thermal atmospheric pressure plasma induces selective cancer cell apoptosis by modulating redox homeostasis
Ju Hyun Yun1, Yoon Hee Yang2, Chang Hak Han3
1Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Ewha Womans University, Seoul, Korea, 07985.
Background:
Anticancer treatments aim to selectively target cancer cells without harming normal cells. While non-thermal atmospheric pressure plasma (NTAPP) has shown anticancer potential across various studies, the mechanisms behind its selective action on cancer cells remain inadequately understood. This study explores the mechanism of NTAPP-induced selective cell death and assesses its application in cancer therapy.
Methods:
We treated HT1080 fibrosarcoma cells with NTAPP and assessed the intracellular levels of mitochondria-derived reactive oxygen species (ROS), mitochondrial function, and cell death mechanisms. We employed N-acetylcysteine to investigate ROS's role in NTAPP-induced cell death. Additionally, single-cell RNA sequencing was used to compare gene expression in NTAPP-treated HT1080 cells and human normal fibroblasts (NF). Western blotting and immunofluorescence staining examined the expression and nuclear translocation of nuclear factor erythroid 2-related factor 2 (NRF2), a key antioxidant gene transcription factor. We also evaluated autophagy activity through fluorescence staining and transmission electron microscopy.
Results:
NTAPP treatment increased ROS levels and induced mitochondrial dysfunction, leading to apoptosis in HT1080 cells. The involvement of ROS in selective cancer cell death was confirmed by N-acetylcysteine treatment. Distinct gene expression patterns were observed between NTAPP-treated NF and HT1080 cells, with NF showing upregulated antioxidant gene expression. Notably, NRF2 expression and nuclear translocation increased in NF but not in HT1080 cells. Furthermore, autophagy activity was significantly higher in normal cells compared to cancer cells.
Conclusions:
Our study demonstrates that NTAPP induces selective cell death in fibrosarcoma cells through the downregulation of the NRF2-induced ROS scavenger system and inhibition of autophagy. These findings suggest NTAPP's potential as a cancer therapy that minimizes damage to normal cells while effectively targeting cancer cells.
Insights
Non-thermal atmospheric pressure plasma (NTAPP) selectively kills fibrosarcoma cells by downregulating the antioxidant NRF2 system and inhibiting autophagy. This cancer therapy minimizes damage to normal cells, offering a promising approach for selective cancer treatment.
Area of Science:
- Biomedical Engineering
- Plasma Medicine
- Cancer Research
Background:
- Non-thermal atmospheric pressure plasma (NTAPP) shows anticancer potential.
- Mechanisms of NTAPP's selective cancer cell targeting are not fully understood.
Purpose of the Study:
- To explore NTAPP-induced selective cell death mechanisms.
- To assess NTAPP's potential in cancer therapy.
Main Methods:
- HT1080 fibrosarcoma cells treated with NTAPP.
- Assessed reactive oxygen species (ROS), mitochondrial function, and cell death.
- Investigated ROS role using N-acetylcysteine.
- Single-cell RNA sequencing compared gene expression in cancer cells and normal fibroblasts (NF).
- Examined NRF2 expression and nuclear translocation.
- Evaluated autophagy activity.
Main Results:
- NTAPP increased ROS and induced apoptosis in cancer cells.
- Normal cells showed upregulated antioxidant gene expression and increased NRF2.
- Autophagy activity was higher in normal cells than cancer cells.
Conclusions:
- NTAPP induces selective fibrosarcoma cell death.
- Mechanism involves downregulation of NRF2-mediated ROS scavenging and autophagy inhibition.
- NTAPP offers potential for cancer therapy with minimal normal cell damage.
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