Abstract
Non-thermal atmospheric plasma (NTAP) has been proven to be an effective anti-tumor tool, with various biological effects such as inhibiting tumor proliferation, metastasis, and promoting tumor cell apoptosis. At present, the main conclusion is that ROS and RNS are the main effector components of NTAP, but the mechanisms of which still lack systematic summary. Therefore, in this review, we first summarized the mechanism by which NTAP directly or indirectly causes an increase in intracellular RONS concentration, and the multiple pathways dysregulation (i.e. NRF2, PI3K, MAPK, NF-κB) induced by intracellular RONS. Then, we generalized the relationship between NTAP induced pathways dysregulation and the various biological effects it brought. The summary of the anti-tumor mechanism of NTAP is helpful for its further research and clinical transformation.
HIGHLIGHTS
Non-thermal atmospheric plasma (NTAP) acts on NADPH oxidase and catalase.
The feeding gas and parameters of NTAP affect its impacts on the signaling pathways.
The impacts of NTAP and RONS on pathways are not always consistent.
NTAP can trigger various anti-tumor biological effects.
Acknowledgments
This work is funded by the National Natural Science Foundation of China (52003112), the College Students’ Innovation and Entrepreneurship Competition Training Program (National Program-202012121009 & 202212121014, Provincial Program-202212121110, University Program-X202012121387) and the Nanfang Hospital President Foundation (2023A023).
Authors’ contributions
Qi Liu: Conceptualization, Writing - Revising & Editing, Supervision, Project Administration, Funding Acquisition, Investigation. Wenjie Wang: Conceptualization, Visualization, Writing – Original Draft, Investigation. Peijia Zheng: Visualization, Writing - Revising & Editing. Liang Yan: Visualization, Writing-Revising & Editing. Xiaomen Chen: Visualization, Writing - Revising & Editing. Zhicheng Wang: Visualization, Writing-Revising & Editing.
Disclosure statement
No potential conflict of interest was reported by the author(s).