Journal
CELLS
Volume 11, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/cells11060930
Keywords
tumor microenvironment; metabolic alterations; tumor therapy; cold atmospheric plasma; tumor spheroids; plasma jet; malignant melanoma; T cell; macrophage
Categories
Funding
- Wilhelm Sander Foundation (2020.132.1)
- Hiege Foundation [200504, CRC1066 (TPB14)]
- DAAD One-Year Research Grant for Doctoral Candidates [57552339]
- BOWA Medical
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The cellular composition of the tumor microenvironment has a significant impact on responses to cancer therapies. This study analyzes the effects of oxidative stress induced by cold atmospheric plasma (CAP) on tumor cells, T cells, and macrophages in melanoma microenvironment. The study found that CAP treatment reduced viability and proliferation of cells, induced cell cycle arrest and apoptosis, and increased mitochondrial stress. CAP treatment also influenced the polarization of macrophages and inhibited the growth of melanoma cells in vitro.
The cellular composition of the tumor microenvironment, including tumor, immune, stromal, and endothelial cells, significantly influences responses to cancer therapies. In this study, we analyzed the impact of oxidative stress, induced by cold atmospheric plasma (CAP), on tumor cells, T cells, and macrophages, which comprise part of the melanoma microenvironment. To accomplish this, cells were grown in different in vitro cell culture models and were treated with varying amounts of CAP. Subsequent alterations in viability, proliferation, and phenotype were analyzed via flow cytometry and metabolic alterations by Seahorse Cell Mito Stress Tests. It was found that cells generally exhibited reduced viability and proliferation, stemming from CAP induced G2/M cell cycle arrest and subsequent apoptosis, as well as increased mitochondrial stress following CAP treatment. Overall, sensitivity to CAP treatment was found to be cell type dependent with T cells being the most affected. Interestingly, CAP influenced the polarization of M0 macrophages to a M0/M2-like phenotype, and M1 macrophages were found to display a heightened sensitivity to CAP induced mitochondrial stress. CAP also inhibited the growth and killed melanoma cells in 2D and 3D in vitro cell culture models in a dose-dependent manner. Improving our understanding of oxidative stress, mechanisms to manipulate it, and its implications for the tumor microenvironment may help in the discovery of new therapeutic targets.
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