Abstract
The aim of this study is to investigate the effects of cold atmospheric pressure plasma (CAP)-induced radicals on the epidermal growth factor receptor (EGFR), which is overexpressed by oral squamous cell carcinoma, to determine the underlying mechanism of selective killing. CAP-induced highly reactive radicals were observed in both plasma plume and cell culture media. The selective killing effect was observed in oral squamous cell carcinoma compared with normal human gingival fibroblast. Degradation and dysfunction of EGFRs were observed only in the EGFR-overexpressing oral squamous cell carcinoma and not in the normal cell. Nitric oxide scavenger pretreatment in cell culture media before CAP treatment rescued above degradation and dysfunction of the EGFR as well as the killing effect in oral squamous cell carcinoma. CAP may be a promising cancer treatment method by inducing EGFR dysfunction in EGFR-overexpressing oral squamous cell carcinoma via nitric oxide radicals.
Highlights
Cold atmospheric pressure plasma (CAP) is a promising therapy to selectively eradicate cancer cells [1,2]
The quantity and type of CAP-induced radicals generated were analyzed by collecting optical emission spectrum off of the solutions treated by CAP
We found that CAP treatment led to degradation and dephosphorylation of epidermal growth factor receptor (EGFR) in HSC-2 cells, which suggested a deactivation of the EGFR pathway
Summary
Cold atmospheric pressure plasma (CAP) is a promising therapy to selectively eradicate cancer cells [1,2]. CAP damages cancer cells intracellularly such as damaging deoxyribonucleic acid, mitochondria and causing apoptosis of the treated cells [3,4,5]. These changes are mostly explained by the accumulation of intracellular reactive oxygen species (ROS) in cancer cells, which induces mitochondrial dysfunction, sub-G1 phase arrest and deoxyribonucleic acid damage [6,7]. Cancer cells are more vulnerable to accumulation of ROS due to their elevated rates of ROS production, where they promote.
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