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The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma. / Biryukov, Mikhail; Semenov, Dmitriy; Kryachkova, Nadezhda et al.

In: Biomolecules, Vol. 13, No. 11, 1672, 20.11.2023.

Research output: Contribution to journalArticlepeer-review

Harvard

Biryukov, M, Semenov, D, Kryachkova, N, Polyakova, A, Patrakova, E, Troitskaya, O, Milakhina, E, Poletaeva, J, Gugin, P, Ryabchikova, E, Zakrevsky, D, Schweigert, I & Koval, O 2023, 'The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma', Biomolecules, vol. 13, no. 11, 1672. https://doi.org/10.3390/biom13111672

APA

Biryukov, M., Semenov, D., Kryachkova, N., Polyakova, A., Patrakova, E., Troitskaya, O., Milakhina, E., Poletaeva, J., Gugin, P., Ryabchikova, E., Zakrevsky, D., Schweigert, I., & Koval, O. (2023). The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma. Biomolecules, 13(11), [1672]. https://doi.org/10.3390/biom13111672

Vancouver

Biryukov M, Semenov D, Kryachkova N, Polyakova A, Patrakova E, Troitskaya O et al. The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma. Biomolecules. 2023 Nov 20;13(11):1672. doi: 10.3390/biom13111672

Author

Biryukov, Mikhail ; Semenov, Dmitriy ; Kryachkova, Nadezhda et al. / The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma. In: Biomolecules. 2023 ; Vol. 13, No. 11.

BibTeX

@article{a539a566183b48d789eae9a5b461eaf2,
title = "The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma",
abstract = "The interaction of cold atmospheric plasma (CAP) with biotargets is accompanied by chemical reactions on their surfaces and insides, and it has great potential as an anticancer approach. This study discovers the molecular mechanisms that may explain the selective death of tumor cells under CAP exposure. To reach this goal, the transcriptional response to CAP treatment was analyzed in A549 lung adenocarcinoma cells and in lung-fibroblast Wi-38 cells. We found that the CAP treatment induced the common trend of response from A549 and Wi-38 cells-the p53 pathway, KRAS signaling, UV response, TNF-alpha signaling, and apoptosis-related processes were up-regulated in both cell lines. However, the amplitude of the response to CAP was more variable in the A549 cells. The CAP-dependent death of A549 cells was accompanied by DNA damage, cell-cycle arrest in G2/M, and the dysfunctional response of glutathione peroxidase 4 (GPx4). The activation of the genes of endoplasmic reticulum stress and ER lumens was detected only in the A549 cells. Transmission-electron microscopy confirmed the alteration of the morphology of the ER lumens in the A549 cells after the CAP exposure. It can be concluded that the responses to nuclear stress and ER stress constitute the main differences in the sensitivity of tumor and healthy cells to CAP exposure.",
author = "Mikhail Biryukov and Dmitriy Semenov and Nadezhda Kryachkova and Alina Polyakova and Ekaterina Patrakova and Olga Troitskaya and Elena Milakhina and Julia Poletaeva and Pavel Gugin and Elena Ryabchikova and Dmitriy Zakrevsky and Irina Schweigert and Olga Koval",
note = "This research was funded by Russian Science Foundation, grant number #22-49-08003. Публикация для корректировки.",
year = "2023",
month = nov,
day = "20",
doi = "10.3390/biom13111672",
language = "English",
volume = "13",
journal = "Biomolecules",
issn = "2218-273X",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "11",

}

RIS

TY - JOUR

T1 - The Molecular Basis for Selectivity of the Cytotoxic Response of Lung Adenocarcinoma Cells to Cold Atmospheric Plasma

AU - Biryukov, Mikhail

AU - Semenov, Dmitriy

AU - Kryachkova, Nadezhda

AU - Polyakova, Alina

AU - Patrakova, Ekaterina

AU - Troitskaya, Olga

AU - Milakhina, Elena

AU - Poletaeva, Julia

AU - Gugin, Pavel

AU - Ryabchikova, Elena

AU - Zakrevsky, Dmitriy

AU - Schweigert, Irina

AU - Koval, Olga

N1 - This research was funded by Russian Science Foundation, grant number #22-49-08003. Публикация для корректировки.

PY - 2023/11/20

Y1 - 2023/11/20

N2 - The interaction of cold atmospheric plasma (CAP) with biotargets is accompanied by chemical reactions on their surfaces and insides, and it has great potential as an anticancer approach. This study discovers the molecular mechanisms that may explain the selective death of tumor cells under CAP exposure. To reach this goal, the transcriptional response to CAP treatment was analyzed in A549 lung adenocarcinoma cells and in lung-fibroblast Wi-38 cells. We found that the CAP treatment induced the common trend of response from A549 and Wi-38 cells-the p53 pathway, KRAS signaling, UV response, TNF-alpha signaling, and apoptosis-related processes were up-regulated in both cell lines. However, the amplitude of the response to CAP was more variable in the A549 cells. The CAP-dependent death of A549 cells was accompanied by DNA damage, cell-cycle arrest in G2/M, and the dysfunctional response of glutathione peroxidase 4 (GPx4). The activation of the genes of endoplasmic reticulum stress and ER lumens was detected only in the A549 cells. Transmission-electron microscopy confirmed the alteration of the morphology of the ER lumens in the A549 cells after the CAP exposure. It can be concluded that the responses to nuclear stress and ER stress constitute the main differences in the sensitivity of tumor and healthy cells to CAP exposure.

AB - The interaction of cold atmospheric plasma (CAP) with biotargets is accompanied by chemical reactions on their surfaces and insides, and it has great potential as an anticancer approach. This study discovers the molecular mechanisms that may explain the selective death of tumor cells under CAP exposure. To reach this goal, the transcriptional response to CAP treatment was analyzed in A549 lung adenocarcinoma cells and in lung-fibroblast Wi-38 cells. We found that the CAP treatment induced the common trend of response from A549 and Wi-38 cells-the p53 pathway, KRAS signaling, UV response, TNF-alpha signaling, and apoptosis-related processes were up-regulated in both cell lines. However, the amplitude of the response to CAP was more variable in the A549 cells. The CAP-dependent death of A549 cells was accompanied by DNA damage, cell-cycle arrest in G2/M, and the dysfunctional response of glutathione peroxidase 4 (GPx4). The activation of the genes of endoplasmic reticulum stress and ER lumens was detected only in the A549 cells. Transmission-electron microscopy confirmed the alteration of the morphology of the ER lumens in the A549 cells after the CAP exposure. It can be concluded that the responses to nuclear stress and ER stress constitute the main differences in the sensitivity of tumor and healthy cells to CAP exposure.

UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85177732828&origin=inward&txGid=58f2cf604522ce92ac58bdafa3698bec

U2 - 10.3390/biom13111672

DO - 10.3390/biom13111672

M3 - Article

C2 - 38002354

VL - 13

JO - Biomolecules

JF - Biomolecules

SN - 2218-273X

IS - 11

M1 - 1672

ER -

ID: 59228021