scholarly journals Combined metformin and resveratrol confers protection against UVC-induced DNA damage in A549 lung cancer cells via modulation of cell cycle checkpoints and DNA repair

2016 ◽  
Vol 35 (6) ◽  
pp. 3735-3741 ◽  
Author(s):  
YONG-SYU LEE ◽  
BARBARA B. DOONAN ◽  
JOSEPH M. WU ◽  
TZE-CHEN HSIEH
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Cancer Cells ◽  
Cell Cycle Checkpoints ◽  
Lung Cancer Cells ◽  
A549 Lung

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

2010 ◽  
Vol 29 (7) ◽  
pp. 607-614 ◽  
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.

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

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.

Cantharidin induces DNA damage and inhibits DNA repair-associated protein levels in NCI-H460 human lung cancer cells

2014 ◽  
Vol 30 (10) ◽  
pp. 1135-1143 ◽  
Author(s):  
Te-Chun Hsia ◽  
Ju-Hwa Lin ◽  
Shu-Chun Hsu ◽  
Nou-Ying Tang ◽  
Hsu-Feng Lu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Dna Repair ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Protein Levels ◽  
Human Lung Cancer Cells

Effects of 7-hydroxy-3-methoxycadalene on cell cycle, apoptosis and protein translation in A549 lung cancer cells

BioFactors ◽  
2007 ◽  
Vol 29 (2-3) ◽  
pp. 67-75 ◽  
Author(s):  
Hua Jin ◽  
Hyun-Woo Kim ◽  
Cheng-Xiong Xu ◽  
Jung-Taek Kwon ◽  
Soon-Kyung Hwang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Protein Translation ◽  
Lung Cancer Cells ◽  
A549 Lung

scholarly journals Anti-proliferation effect of Scutellaria barbata D. Don extract on lung cancer

2021 ◽  
Vol 18 (9) ◽  
pp. 1867-1872
Author(s):  
Zhang Hu ◽  
Duan Jing
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Blue Staining ◽  
G1 Phase ◽  
Scutellaria Barbata ◽  
A549 Lung

Purpose: To investigate the effect of Scutellaria barbata D. Don extract (SBDE) on apoptosis and proliferation in A549 human lung cancer cells. Methods: Inverted microscope was used to observe morphological changes in A549 cells after exposure to SBDE. Trypan blue staining of living cells was applied to construct cell growth curve after treatment with varying concentrations of SBDE. The influence of SBDE on cell proliferation, apoptosis and cell cycle was determined by MTT assay while protein expressions of key apoptosis-related enzymes were evaluated by immuno-cytochemical method. Results: SBDE inhibited the growth of A549 lung cancer cells at a concentration range of 20 - 160 μg/mL. Flow cytometry showed that SBDE induced apoptosis in the A549 cells. The proportion of cells in G0/G1-phase increased significantly (p < 0.01), while the proportion of cells in S-phase and G2/Mphase decreased correspondingly, indicating that the cells were in G0/G1-phase arrest. Cell cycle arrest and apoptosis-inducing effect gradually increased with increase in SBDE concentration. With increasing concentrations of SBDE, there were significant increases in the expressions of caspase-3 (p < 0.05), caspase-8 (p < 0.01) and caspase-9 (p < 0.05), and significant decreases in Ki-67 (p < 0.01) and p21 ras protein (p < 0.01). Conclusion: SBDE exerts significant inhibitory effect on the proliferation of A549 lung cancer cells, which can be developed for the treatment of lung cancer patients.

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