Oxidative stress facilitates IFN-γ-induced mimic extracellular trap cell death in A549 lung epithelial cancer cells

Chiou-Feng Lin; Chia-Ling Chen; Shun Yi Chien; Po Chun Tseng; Yu Chih Wang; Tsung Ting Tsai

doi:10.1371/journal.pone.0162157

Oxidative stress facilitates IFN-γ-induced mimic extracellular trap cell death in A549 lung epithelial cancer cells

Chiou-Feng Lin, Chia-Ling Chen, Shun Yi Chien, Po Chun Tseng, Yu Chih Wang, Tsung Ting Tsai

Research output: Contribution to journal › Article › peer-review

6 Citations (Scopus)

Abstract

We previously demonstrated that IFN-γ induces an autophagy-regulated mimic extracellular trap cell death (ETosis) in A549 human lung cancer cells. Regarding reactive oxygen species (ROS) are involved in ETosis, this study investigated the role of oxidative stress. After IFN-γ stimulation, a necrosis-like cell death mimic ETosis occurred accompanied by the inhibition of cell growth, aberrant nuclear staining, and nucleosome release. ROS were generated in a time-dependent manner with an increase in NADPH oxidase component protein expression. STAT1-mediated IFN regulatory factor-1 activation was essential for upregulating ROS production. By genetically silencing p47^phox, IFN-γ-induced ROS and mimic ETosis were significantly attenuated. This mechanistic study indicated that ROS may mediate DNA damage followed by histone H3 citrullination. Furthermore, ROS promoted IFN-γ-induced mimic ETosis in cooperation with autophagy. These findings further demonstrate that ROS regulates IFN-γ-induced mimic ETosis in lung epithelial malignancy.

Original language	English
Article number	e0162157
Journal	PLoS One
Volume	11
Issue number	8
DOIs	https://doi.org/10.1371/journal.pone.0162157
Publication status	Published - Aug 1 2016

ASJC Scopus subject areas

Medicine(all)
Biochemistry, Genetics and Molecular Biology(all)
Agricultural and Biological Sciences(all)

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This output contributes to the following UN Sustainable Development Goals (SDGs)

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title = "Oxidative stress facilitates IFN-γ-induced mimic extracellular trap cell death in A549 lung epithelial cancer cells",

abstract = "We previously demonstrated that IFN-γ induces an autophagy-regulated mimic extracellular trap cell death (ETosis) in A549 human lung cancer cells. Regarding reactive oxygen species (ROS) are involved in ETosis, this study investigated the role of oxidative stress. After IFN-γ stimulation, a necrosis-like cell death mimic ETosis occurred accompanied by the inhibition of cell growth, aberrant nuclear staining, and nucleosome release. ROS were generated in a time-dependent manner with an increase in NADPH oxidase component protein expression. STAT1-mediated IFN regulatory factor-1 activation was essential for upregulating ROS production. By genetically silencing p47phox, IFN-γ-induced ROS and mimic ETosis were significantly attenuated. This mechanistic study indicated that ROS may mediate DNA damage followed by histone H3 citrullination. Furthermore, ROS promoted IFN-γ-induced mimic ETosis in cooperation with autophagy. These findings further demonstrate that ROS regulates IFN-γ-induced mimic ETosis in lung epithelial malignancy.",

author = "Chiou-Feng Lin and Chia-Ling Chen and Chien, {Shun Yi} and Tseng, {Po Chun} and Wang, {Yu Chih} and Tsai, {Tsung Ting}",

note = "Funding Information: This work was supported by grant NHRI-EX102-9917NC from the National Health Research Institutes, Taiwan and grant MOST100-2320-B-006-009-MY3 from the Ministry of Science and Technology, Taiwan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: {\textcopyright} 2016 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.",

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doi = "10.1371/journal.pone.0162157",

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AU - Lin, Chiou-Feng

AU - Chen, Chia-Ling

AU - Chien, Shun Yi

AU - Tseng, Po Chun

AU - Wang, Yu Chih

AU - Tsai, Tsung Ting

N1 - Funding Information: This work was supported by grant NHRI-EX102-9917NC from the National Health Research Institutes, Taiwan and grant MOST100-2320-B-006-009-MY3 from the Ministry of Science and Technology, Taiwan. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Publisher Copyright: © 2016 Lin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PY - 2016/8/1

Y1 - 2016/8/1

N2 - We previously demonstrated that IFN-γ induces an autophagy-regulated mimic extracellular trap cell death (ETosis) in A549 human lung cancer cells. Regarding reactive oxygen species (ROS) are involved in ETosis, this study investigated the role of oxidative stress. After IFN-γ stimulation, a necrosis-like cell death mimic ETosis occurred accompanied by the inhibition of cell growth, aberrant nuclear staining, and nucleosome release. ROS were generated in a time-dependent manner with an increase in NADPH oxidase component protein expression. STAT1-mediated IFN regulatory factor-1 activation was essential for upregulating ROS production. By genetically silencing p47phox, IFN-γ-induced ROS and mimic ETosis were significantly attenuated. This mechanistic study indicated that ROS may mediate DNA damage followed by histone H3 citrullination. Furthermore, ROS promoted IFN-γ-induced mimic ETosis in cooperation with autophagy. These findings further demonstrate that ROS regulates IFN-γ-induced mimic ETosis in lung epithelial malignancy.

AB - We previously demonstrated that IFN-γ induces an autophagy-regulated mimic extracellular trap cell death (ETosis) in A549 human lung cancer cells. Regarding reactive oxygen species (ROS) are involved in ETosis, this study investigated the role of oxidative stress. After IFN-γ stimulation, a necrosis-like cell death mimic ETosis occurred accompanied by the inhibition of cell growth, aberrant nuclear staining, and nucleosome release. ROS were generated in a time-dependent manner with an increase in NADPH oxidase component protein expression. STAT1-mediated IFN regulatory factor-1 activation was essential for upregulating ROS production. By genetically silencing p47phox, IFN-γ-induced ROS and mimic ETosis were significantly attenuated. This mechanistic study indicated that ROS may mediate DNA damage followed by histone H3 citrullination. Furthermore, ROS promoted IFN-γ-induced mimic ETosis in cooperation with autophagy. These findings further demonstrate that ROS regulates IFN-γ-induced mimic ETosis in lung epithelial malignancy.

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Oxidative stress facilitates IFN-γ-induced mimic extracellular trap cell death in A549 lung epithelial cancer cells

Abstract

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