Journal
CANCERS
Volume 12, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/cancers12051280
Keywords
cholangiocarcinoma; cold plasma; innovative therapy; tumor cells; macrophages; plasma selectivity; plasma jet
Categories
Funding
- LABEX PLAS@PAR [ANR-11-IDEX-0004-02]
- LABEXPlas@parproject
- Agence NationaledelaRecherche,as part of the programme Investissementsd'avenir [ANR-11-IDEX-0004-02]
- programEmergence@Sorbonne Universite 2016
- French Ministry of Solidarity and Health
- Inserm [INCA-DGOS-Inserm_12560]
- Region Ile-de-France [16016309]
- Platform program of Sorbonne Universite
- le programme Emergence 2019 Canceropole Ile de France et le programmeAmorcage 2019 SiRIC Curamus [ASCLEPIOS 193602, PROMISE 195741]
- et le programmeAmorcage 2019 SiRIC Curamus [PROMISE 195741]
- Agence Nationale de la Recherche [ANR-17-CE14-0013-01]
- Fondation pour la Recherche Medicale [FRM SPF201809007054]
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Through the last decade, cold atmospheric plasma (CAP) has emerged as an innovative therapeutic option for cancer treatment. Recently, we have set up a potentially safe atmospheric pressure plasma jet device that displays antitumoral properties in a preclinical model of cholangiocarcinoma (CCA), a rare and very aggressive cancer emerging from the biliary tree with few efficient treatments. In the present study, we aimed at deciphering the molecular mechanisms underlying the antitumor effects of CAP towards CCA in both an in vivo and in vitro context. In vivo, using subcutaneous xenografts into immunocompromised mice, CAP treatment of CCA induced DNA lesions and tumor cell apoptosis, as evaluated by 8-oxoguanine and cleaved caspase-3 immunohistochemistry, respectively. The analysis of the tumor microenvironment showed changes in markers related to macrophage polarization. In vitro, the incubation of CCA cells with CAP-treated culture media (i.e., plasma-activated media, PAM) led to a dose response decrease in cell survival. At molecular level, CAP treatment induced double-strand DNA breaks, followed by an increased phosphorylation and activation of the cell cycle master regulators CHK1 and p53, leading to cell cycle arrest and cell death by apoptosis. In conclusion, CAP is a novel therapeutic option to consider for CCA in the future.
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