Format

Send to

Choose Destination
Sci Rep. 2017 Jan 25;7:41163. doi: 10.1038/srep41163.

Mechanistic insights into the impact of Cold Atmospheric Pressure Plasma on human epithelial cell lines.

Author information

1
IPREM, UMR 5254, Université de Pau et des Pays de l'Adour, 64000, Pau, France.
2
STROMALAB, Université de Toulouse, CNRS ERL5311, EFS, INP-ENVT, UPS, INSERM U1031, BP31432 Toulouse cedex 4, France.
3
Univ. BORDEAUX, ISM. CNRS UMR 5255 NSysA group, ENSCBP, Pessac, 33607, France.
4
Institut de Pharmacologie et de Biologie Structurale, Université de Toulouse, CNRS, UPS, France.
5
Genoskin, Centre Pierre Potier-Oncopole, F-31106 Toulouse, France.

Abstract

Compelling evidence suggests that Cold Atmospheric Pressure Plasma (CAPP) has potential as a new cancer therapy. However, knowledge about cellular signaling events and toxicity subsequent to plasma treatment is still poorly documented. The aim of this study was to focus on the interaction between 3 different types of plasma (He, He-O2, He-N2) and human epithelial cell lines to gain better insight into plasma-cell interaction. We provide evidence that reactive oxygen and nitrogen species (RONS) are inducing cell death by apoptosis and that the proteasome, a major intracellular proteolytic system which is important for tumor cell growth and survival, is a target of (He or He-N2) CAPP. However, RONS are not the only actors involved in cell death; electric field and charged particles could play a significant role especially for He-O2 CAPP. By differential label-free quantitative proteomic analysis we found that CAPP triggers antioxidant and cellular defense but is also affecting extracellular matrix in keratinocytes. Moreover, we found that malignant cells are more resistant to CAPP treatment than normal cells. Taken together, our findings provide insight into potential mechanisms of CAPP-induced proteasome inactivation and the cellular consequences of these events.

PMID:
28120925
PMCID:
PMC5264585
DOI:
10.1038/srep41163
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center