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

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 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.

scholarly journals Middle Infrared Radiation Induces G2/M Cell Cycle Arrest in A549 Lung Cancer Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (1) ◽  
pp. e54117 ◽  
Author(s):  
Hsin-Yi Chang ◽  
Meng-Her Shih ◽  
Hsuan-Cheng Huang ◽  
Shang-Ru Tsai ◽  
Hsueh-Fen Juan ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Infrared Radiation ◽  
Lung Cancer Cells ◽  
M Cell ◽  
Cycle Arrest ◽  
Middle Infrared ◽  
A549 Lung

scholarly journals Forsythia suspensa extract has inhibitory effect on proliferation and apoptosis of A549 lung cancer cells

2021 ◽  
Vol 18 (9) ◽  
pp. 1949-1954
Author(s):  
Wei-guo Zhang ◽  
Qin Liu ◽  
Cai-peng Lei
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
A549 Cells ◽  
Inhibitory Effect ◽  
Lung Cancer Cells ◽  
Blue Staining ◽  
G1 Phase ◽  
Forsythia Suspensa ◽  
A549 Lung

Purpose: To investigate the effect of Forsythia suspensa extract (FSE) on apoptosis and proliferation in A549 human lung cancer cells. Methods: Inverted microscope was employed to observe morphological changes in A549 cells after exposure to FSE. Trypan blue staining of living cells was used to construct the cell growth curve after treatment with varying concentrations of FSE. The influence of FSE on cell proliferation, apoptosis and cell cycle was determined by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, while protein expressions of key apoptosis-related enzymes were evaluated by immunocytochemical method. Results: FSE inhibited the growth of A549 lung cancer cells at a concentration range of 10 - 150 μg/mL. Flow cytometry results showed that FSE induced apoptosis in A549 cells. The proportion of cells in G0/G1-phase increased significantly (p < 0.01), while the proportion of cells in S- and G2/M-phase decreased correspondingly, indicating that the cells were in G0/G1-phase arrest. Cell cycle arrest and apoptosis-inducing effect gradually rose with increase in FSE concentration. With increasing concentrations of FSE, there was also significant increase in the expressions of caspase-3 (p < 0.05), caspase-8 (p < 0.01) and caspase-9 (p < 0.05), but significant decrease in Ki-67 (p < 0.01) and p21 ras protein (p < 0.01). Conclusion: FSE exerts significant inhibitory effect on the proliferation of A549 lung cancer cells. Therefore, the plant can potentially be developed for the treatment of lung cancer.

Peniciketal A, A Novel Spiroketal Compound, Exerts Anticancer Effects by Inhibiting Cell Proliferation, Migration and Invasion of A549 Lung Cancer Cells

2019 ◽  
Vol 18 (11) ◽  
pp. 1573-1581 ◽  
Author(s):  
Xue Gao ◽  
Yuming Zhou ◽  
Xiaoqi Zheng ◽  
Hongliu Sun ◽  
Jing Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Lung Cancer Cells ◽  
Normal Fibroblast ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Anticancer Effects ◽  
A549 Lung

Background: Peniciketal A (Pe-A) is a spiroketal compound isolated from saline soil-derived fungus Penicillium raistrickii. However, its role for biological processes has not been clarified. In this study, we for the first time investigated the anticancer effects and the underlying mechanisms of Pe-A in A549 lung cancer cells. Metheds: Cell proliferation was tested by MTT assay and colony formation assay. Flow cytometry was performed to examine the cell cycle, apoptosis and mitochondrial membrane potential. Invasion and migration were analyzed using transwell assay and wound healing analysis. Immunofluorescence staining and western blotting were used to evaluate the protein expression. Results: Pe-A effectively inhibited proliferation, with IC50 values was 22.33 μM for 72 h. Mechanistic studies revealed that Pe-A caused cell cycle arrest at the G0-G1 phase by decreasing cyclinD1 expression and induced apoptosis through accelerating the mitochondrial apoptotic pathway. Moreover, Pe-A significantly inhibited A549 cell migration and invasion by reducing the protein levels of MMP-2 and MMP-9, while the Epithelial- Mesenchymal Transition (EMT) property was also changed. Importantly, Pe-A exhibited much lower toxicity towards L02, normal liver cells, and MRC5, normal fibroblast cells, compared to A549 cells. Conclusion: Collectively, the current results indicate that Pe-A may offer effective potentials and insights for lung cancer treatment and drug design.

scholarly journals 18β-Glycyrrhetinic Acid Has Anti-Cancer Effects via Inducing Apoptosis and G2/M Cell Cycle Arrest, and Inhibiting Migration of A549 Lung Cancer Cells

2021 ◽  
Vol Volume 14 ◽  
pp. 5131-5144
Author(s):  
Ying-Hua Luo ◽  
Cheng Wang ◽  
Wan-Ting Xu ◽  
Yu Zhang ◽  
Tong Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cancer Cells ◽  
Glycyrrhetinic Acid ◽  
Lung Cancer Cells ◽  
M Cell ◽  
Cycle Arrest ◽  
Anti Cancer ◽  
A549 Lung
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