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Published on: June 9, 2023
Selective effects of non-thermal atmospheric plasma on triple-negative breast normal and carcinoma cells through
Yuan Liu1, Sheng Tan2,3, Hao Zhang1
1School of Life Science, University of Science and Technology of China, Hefei, Anhui, 230027, China.
Abstract:
Non-thermal atmospheric plasma (NTP) has shown its selective anticancer effects in many types of tumors in vitro and one of the main mechanisms is that the different increase of intracellular ROS in cancer and homologous normal cells. In this study, we report that NTP treatment reduces the proliferation in triple negative breast cancer (TNBC) and normal cell lines. Simultaneously, STAT3 pathway is inhibited by NTP effects. However, it is observed that normal cells MCF10A are more sensitive to ROS toxicity induced by NTP than cancer cells MDA-MB-231. When 5 mM of ROS inhibitor N-acetyl cysteine (NAC) is employed in NTP treatments, the proliferation of normal breast cells MCF10A recovers. Meanwhile, NTP effects remain significant inhibition of MDA-MB-231 cells. Our results further reveal that NTP can induce apoptosis in MDA-MB-231 cells through inhibiting interleukin-6 receptor (IL-6R) pathway. Moreover, the mechanism of NTP anti-cancer selectivity relates to constantly HER2/Akt activation induced by NTP especially in MCF10A cells but not in MDA-MB-231 cells. Therefore, these two different cell signaling pathways induced by NTP treatments in TNBC and homologous normal cells make NTP becoming a potential tool in future therapy.
Insights
Non-thermal atmospheric plasma (NTP) selectively targets triple-negative breast cancer cells by inhibiting the STAT3 pathway. NTP shows potential as a cancer therapy by inducing apoptosis in cancer cells while sparing normal cells.
Area of Science:
- Biomedical Engineering
- Oncology
- Plasma Physics
Background:
- Non-thermal atmospheric plasma (NTP) exhibits selective anticancer effects via differential reactive oxygen species (ROS) induction.
- Triple-negative breast cancer (TNBC) remains a challenging malignancy with limited therapeutic options.
Purpose of the Study:
- To investigate the selective anticancer effects of NTP on TNBC and normal breast cell lines.
- To elucidate the underlying molecular mechanisms, including STAT3 and IL-6R pathways, and ROS sensitivity.
Main Methods:
- Treatment of MDA-MB-231 (TNBC) and MCF10A (normal) cells with NTP.
- Assessment of cell proliferation and apoptosis.
- Inhibition of ROS using N-acetyl cysteine (NAC).
- Analysis of STAT3, IL-6R, and HER2/Akt signaling pathways.
Main Results:
- NTP inhibited proliferation in both TNBC and normal cells, with normal cells showing higher ROS sensitivity.
- NAC treatment rescued normal cell proliferation while maintaining NTP's effect on cancer cells.
- NTP induced apoptosis in MDA-MB-231 cells by inhibiting the IL-6R pathway.
- Differential activation of HER2/Akt pathways by NTP in normal versus cancer cells contributed to selectivity.
Conclusions:
- NTP demonstrates selective anticancer effects against TNBC, attributed to differential ROS sensitivity and distinct pathway modulation.
- NTP inhibits STAT3 and IL-6R pathways in cancer cells and differentially affects HER2/Akt signaling, supporting its potential as a targeted cancer therapy.
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