Miniature Dielectric Barrier Discharge Nonthermal Plasma Induces Apoptosis in Lung Cancer Cells and Inhibits Cell Migration

Traditional cancer treatments like radiotherapy and chemotherapy have drawbacks and are not selective for killing only cancer cells. Nonthermal atmospheric pressure plasmas with dielectric barrier discharge (DBD) can be applied to living cells and tissues and have emerged as novel tools for localized cancer therapy. The purpose of this study was to investigate the different effects caused by miniature DBD (mDBD) plasma to A549 lung cancer cells. In this study, A549 lung cancer cells cultured in 12 well plates were treated with mDBD plasma for specified treatment times to assess the changes in the size of the area of cell detachment, the viability of attached or detached cells, and cell migration. Furthermore, we investigated an innovative mDBD plasma-based therapy for localized treatment of lung cancer cells through apoptotic induction. Our results indicate that plasma treatment for 120 sec causes apoptotic cell death in 35.8% of cells, while mDBD plasma treatment for 60 sec, 30 sec, or 15 sec causes apoptotic cell death in 20.5%, 14.1%, and 6.3% of the cell population, respectively. Additionally, we observed reduced A549 cell migration in response to mDBD plasma treatment. Thus, mDBD plasma system can be a viable platform for localized lung cancer therapy.

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Momordica charantia L. Induces Non-Apoptotic Cell Death in Human MDA-MB-436 Breast and A549 Lung Cancer Cells by Disrupting Energy Metabolism and Exacerbating Reactive Oxygen Species’ Generation

Journal of Ethnopharmacology ◽

10.1016/j.jep.2021.114036 ◽

2021 ◽

pp. 114036

Author(s):

Adeola Folasade Ehigie ◽

Peng Wei ◽

Taotao Wei ◽

Xiyun Yan ◽

Olufunso O. Olorunsogo ◽

...

Keyword(s):

Lung Cancer ◽

Reactive Oxygen Species ◽

Cell Death ◽

Energy Metabolism ◽

Cancer Cells ◽

Apoptotic Cell ◽

Reactive Oxygen Species Generation ◽

Lung Cancer Cells ◽

Oxygen Species ◽

A549 Lung

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A synthetic 2,3-diarylindole induces cell death via apoptosis and autophagy in A549 lung cancer cells

Bioorganic & Medicinal Chemistry Letters ◽

10.1016/j.bmcl.2016.03.079 ◽

2016 ◽

Vol 26 (9) ◽

pp. 2119-2123 ◽

Cited By ~ 10

Author(s):

Thanya Rukkijakan ◽

Lukana Ngiwsara ◽

Kriengsak Lirdprapamongkol ◽

Jisnuson Svasti ◽

Nared Phetrak ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Lung Cancer Cells ◽

A549 Lung

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Biological Effects of125I Seeds Radiation on A549 Lung Cancer Cells: G2/M Arrest and Enhanced Cell Death

Cancer Investigation ◽

10.3109/07357907.2014.905585 ◽

2014 ◽

Vol 32 (6) ◽

pp. 209-217 ◽

Cited By ~ 19

Author(s):

Ang Qu ◽

Hao Wang ◽

Jinna Li ◽

Junjie Wang ◽

Jingjia Liu ◽

...

Keyword(s):

Lung Cancer ◽

Cell Death ◽

Cancer Cells ◽

Biological Effects ◽

Lung Cancer Cells ◽

A549 Lung

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MG132 as a proteasome inhibitor induces cell growth inhibition and cell death in A549 lung cancer cells via influencing reactive oxygen species and GSH level

Human & Experimental Toxicology ◽

10.1177/0960327109358733 ◽

2010 ◽

Vol 29 (7) ◽

pp. 607-614 ◽

Cited By ~ 15

Author(s):

Yong Hwan Han ◽

Woo Hyun Park

Keyword(s):

Lung Cancer ◽

Reactive Oxygen Species ◽

Cell Cycle ◽

Cell Death ◽

Cancer Cells ◽

Proteasome Inhibitor ◽

A549 Cells ◽

Lung Cancer Cells ◽

Oxygen Species ◽

A549 Lung

Carbobenzoxy-Leu-Leu-leucinal (MG132) as a proteasome inhibitor has been shown to induce apoptotic cell death through formation of reactive oxygen species (ROS). In the present study, we evaluated the effects of MG132 on the growth of A549 lung cancer cells in relation to cell growth, ROS and glutathione (GSH) levels. Treatment with MG132 inhibited the growth of A549 cells with an IC50 of approximately 20 μM at 24 hours. DNA flow cytometric analysis indicated that 0.5 ∼ 30 μM MG132 induced a G1 phase arrest of the cell cycle in A549 cells. Treatment with 10 or 30 μM MG132 also induced apoptosis, as evidenced by sub-G1 cells and annexin V staining cells. This was accompanied by the loss of mitochondrial membrane potential (MMP; Δψm). The intracellular ROS levels including O2•- were strongly increased in 10 or 30 μM MG132-treated A549 cells but were down-regulated in 0.1, 0.5 or 1 μM MG132-treated cells. Furthermore, 10 or 30 μM MG132 increased mitochondrial O2•- level but 0.1, 0.5 or 1 μM MG132 decreased that. In addition, 10 or 30 μM MG132 induced GSH depletion in A549 cells. In conclusion, MG132 inhibited the growth of human A549 cells via inducing the cell cycle arrest as well as triggering apoptosis, which was in part correlated with the changes of ROS and GSH levels. Our present data provide important information on the anti-growth mechanisms of MG132 in A549 lung cancer cells in relation to ROS and GSH.

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Myrcene Exhibits Antitumor Activity Against Lung Cancer Cells by Inducing Oxidative Stress and Apoptosis Mechanisms

Natural Product Communications ◽

10.1177/1934578x20961189 ◽

2020 ◽

Vol 15 (9) ◽

pp. 1934578X2096118

Author(s):

Xudong Bai ◽

Jin Tang

Keyword(s):

Oxidative Stress ◽

Lung Cancer ◽

Dna Damage ◽

Cell Death ◽

Cancer Cells ◽

Metabolic Activity ◽

Lung Cancer Cells ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

A549 Lung

Myrcene, a natural olefinic hydrocarbon, possesses anti-inflammatory, analgesic, antibiotic, and antimutagenic properties, but its anticancer effect has not yet been elucidated. Hence, the present study was framed to investigate the molecular mechanism by which myrcene mediates the anticancer activity of A549 lung adenocarcinoma cells. In vitro, A549 lung cancer cells were cultured either with or without myrcene, and the effects on cellular metabolic activity, levels of reactive oxygen species (ROS), mitochondrial integrity, deoxyribonucleic acid (DNA) damage, and activity of caspases were analyzed. The study demonstrated that compared with control cells, myrcene induces cell death in a dose-dependent manner while inducing ROS levels. Further experiments revealed that the metabolic activity of the A549 lung adenocarcinoma cells was diminished with increased DNA damage and altered cellular integrity. In addition, increased activity of caspase-3 was also evidenced with reduced mitochondrial membrane potential synthesis in the myrcene-treated cells, which demonstrate that lung cancer cells experience signs of toxicity during myrcene treatment through the activation of the apoptosis mechanism via mitochondria-mediated cell death signaling and induction of oxidative stress. The results provide the first report on the evidence of anticancer activity and the possibility of a new drug that could be used for the treatment of lung cancer.

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