Cold atmospheric plasma inhibits the growth of osteosarcoma cells by inducing apoptosis, independent of the device used.

Abstract:

:Osteosarcoma (OS) is the most common tumor of the musculoskeletal system. Recently, cold atmospheric plasma (CAP) has been regarded as a promising anti-oncogenic therapy. Previous experimental studies have demonstrated that CAP treatment results in significant growth inhibition of human sarcoma and is able to induce apoptosis. However, due to device-specific parameters, there is a large variability in the antitumor effects of different CAP sources. In the present study, the cellular effects of CAP treatment from two different CAP devices were investigated and their pro-apoptotic efficacy was characterized. The OS cell lines, U2-OS and MNNG/HOS, were treated with two CAP devices, kINPen MED and MiniJet-R. Control groups were treated with argon. The anti-proliferative effect of each treatment was demonstrated using cell counting and the activation of apoptotic mechanisms was determined using Comet, TUNEL and Caspase-3/Caspase-7 assays. The results revealed that treatment of both OS cell lines with the two CAP sources resulted in significant inhibition of cell growth. Subsequently, the activation of Caspases and the induction of apoptotic DNA fragmentation was demonstrated. The biological effects of each CAP source did not differ significantly. The treatment of OS cells with CAP lead to an induction of apoptosis and a reduction of cell growth. Therefore, the biological effects of CAP appear to be general as the two devices of different design produced highly comparable cell responses. Therefore, the type of device used does not seem to affect the efficacy of CAP-based antitumor therapy.

journal_name

Oncol Lett

journal_title

Oncology letters

authors

Haralambiev L,Wien L,Gelbrich N,Lange J,Bakir S,Kramer A,Burchardt M,Ekkernkamp A,Gümbel D,Stope MB

doi

10.3892/ol.2019.11115

subject

Has Abstract

pub_date

2020-01-01 00:00:00

pages

283-290

issue

1

eissn

1792-1074

issn

1792-1082

pii

OL-0-0-11115

journal_volume

19

pub_type

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