Abstract
Osteosarcoma and Ewing’s sarcoma are the most common malignant bone tumors. Conventional therapies such as polychemotherapy, local surgery, and radiotherapy improve the clinical outcome for patients. However, they are accompanied by acute and chronic side effects that affect the quality of life of patients, motivating novel research lines on therapeutic options for the treatment of sarcomas. Previous experimental work with physical plasma operated at body temperature (cold atmospheric plasma, CAP) demonstrated anti-oncogenic effects on different cancer cell types. This study investigated the anti-cancer effect of CAP on two bone sarcoma entities, osteosarcoma and Ewing’s sarcoma, which were represented by four cell lines (U2-OS, MNNG/HOS, A673, and RD-ES). A time-dependent anti-proliferative effect of CAP on all cell lines was observed. CAP-induced alterations in cell membrane functionality were detected by performing a fluorescein diacetate (FDA) release assay and an ATP release assay. Additionally, modifications of the cell membrane and modifications in the actin cytoskeleton composition were examined using fluorescence microscopy monitoring dextran-uptake assay and G-/F-actin distribution. Furthermore, the CAP-induced induction of apoptosis was determined by TUNEL and active caspases assays. The observations suggest that a single CAP treatment of bone sarcoma cells may have significant anti-oncogenic effects and thus may be a promising extension to existing applications.
Highlights
The most common primary solid malignancy of bone is osteosarcoma (OS)
Previous experimental work with physical plasma operated at body temperature demonstrated anti-oncogenic effects on different cancer cell types
This study investigated the anti-cancer effect of CAP on two bone sarcoma entities, osteosarcoma and Ewing’s sarcoma, which were represented by four cell lines (U2-OS, MNNG/HOS, A673, and RD-ES)
Summary
The most common primary solid malignancy of bone is osteosarcoma (OS). It is characterized by the production of osteoid by malignant mesenchymal cells [1,2]. With the exception of MNNG/HOS cells (103 ± 9%, p = 0.956), a modest but significant increase of the release of fluorescein was detected after CAP treatment (U-2 OS: 107 ± 4%, p = 0.029; A673: 106 ± 6%, p = 0.032; RD-ES: 113 ± 5%, p = 0.025; Figure 3E–H). The selective anti-cancer potential of CAP can be attributed to the combined effect of several cellular factors, such as, for example, the increased expression of membrane channels or the reduced expression of specific antioxidative enzymes in cancer cells [58], and due to the higher sensibility of cancer cells to oxidative stress as a result of their high metabolic rate [56]. Especially in vivo models, will be necessary in the future to answer the possible clinical applications and side effects of CAP treatment in bone sarcomas
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