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. 2022 May 13;9:884887. doi: 10.3389/fmed.2022.884887

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Copyright © 2022 Min, Xie, Ren, Sun, Wang, Dang and Zhang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The effect of cold atmospheric plasma (CAP) on extracellular matrix (ECM) and its molecular mechanism on tumor cells have been studied at present. (1) CAP can inhibit tumor progression by oxidizing or destroying the structure of extracellular matrix (ECM), which includes collagen, hyaluronan, fibronectin, integrin and so on. (2) The cholesterol content of tumor cell membrane is lower than that of non-malignant cells, and it is easier for CAP-derived reactive oxygen and nitrogen species (RONS) to oxidize the lipids on the cell membrane to form pores and enter the cell. (3) Generally, the expression of aquaporin (AQP) in tumor cells increases, which is helpful for the transfer of RONS into cells. (4) With the increase of RONS derived from CAP, the antioxidant defense system of tumor cells is overwhelmed, which limits its protective effect on oxidative stress. (5) The increase of intracellular RONS affects intracellular calcium homeostasis. Through the interaction with inositol triphosphate receptor (IP3-RR) and ryanoid receptor (RR), calcium ions flow into the cytoplasm from endoplasmic reticulum (ER), meanwhile, mitochondrial permeability transition pores (mPTP) are opened to make calcium ions flow into mitochondria through mitochondria-associated ER membranes (MAM), resulting in mitochondrial-dependent apoptosis. (6) The increase of intracellular RONS can activate many different mitogen-activated protein kinase (MAPK) cascades, resulting in cell apoptosis. (7) CAP induces DNA and RNA damage in tumor cells, including DNA single-strand or double-strand break (DSB, SSB), DNA-protein crosslinks (DPC), and chemical modification of DNA and RNA bases, resulting in apoptosis, necrosis and senescence. However, DSB may be the result of apoptosis induced by CAP rather than the direct effect of CAP. (8) The mechanism of other active components of CAP such as charged particles, electric field and ultraviolet radiation on tumor cells needs to be further studied. Created by Biorender.