Curcumin Induces Small Cell Lung Cancer NCI-H446 Cell Apoptosis via the Reactive Oxygen Species-Mediated Mitochondrial Pathway and Not the Cell Death Receptor Pathway

2012 ◽  
Vol 31 (2) ◽  
pp. 139-150 ◽  
Author(s):  
Cheng-Liang Yang ◽  
Ye-Gang Ma ◽  
Yi-Xue Xue ◽  
Yong-Yu Liu ◽  
Hui Xie ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cell Apoptosis ◽  
Death Receptor ◽  
Mitochondrial Pathway ◽  
Small Cell ◽  
Oxygen Species ◽  
Small Cell Lung ◽  
Cell Death Receptor

Curcumin exerts cytotoxicity dependent on reactive oxygen species accumulation in non-small-cell lung cancer cells

2019 ◽  
Vol 15 (11) ◽  
pp. 1243-1253 ◽  
Author(s):  
Cuijuan Wang ◽  
Xingguo Song ◽  
Ming Shang ◽  
Wei Zou ◽  
Mengping Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Reactive Oxygen ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Oxygen Species ◽  
Small Cell Lung

Activation of HGF/c-Met pathway contributes to the reactive oxygen species generation and motility of small cell lung cancer cells

2007 ◽  
Vol 292 (6) ◽  
pp. L1488-L1494 ◽  
Author(s):  
Ramasamy Jagadeeswaran ◽  
Sujatha Jagadeeswaran ◽  
Vytas P. Bindokas ◽  
Ravi Salgia
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Small Cell ◽  
Oxygen Species ◽  
Small Cell Lung ◽  
Met Receptor Tyrosine Kinase

Small cell lung cancer (SCLC) is a difficult disease to treat and sometimes has overexpression or mutation of c-Met receptor tyrosine kinase. The effects of c-Met/hepatocyte growth factor (c-Met/HGF, ligand for c-Met) on activation of reactive oxygen species (ROS) was determined. HGF stimulation of c-Met-overexpressing H69 SCLC cells (40 ng/ml, 15 min) resulted in an increase of ROS, measured with fluorescent probe 2′-7′-dichlorofluorescein diacetate (DCFH-DA) or dihydroethidine (DHE) but not in c-Met-null H446 cells. ROS was increased in juxtamembrane (JM)-mutated variants (R988C and T1010I) of c-Met compared with wild-type c-Met-expressing cells. ROS was significantly inhibited by preincubation of SCLC cells with pyrrolidine dithiocarbamate (PDTC, 100 μM) and/or SU11274 (small molecule c-Met tyrosine kinase inhibitor, 2 μM) for 3 h. PDTC and SU11274 also abrogated the HGF proliferative signal and cell motility in a cooperative fashion. H2O2 treatment of SCLC cells (over 15 min) led to phosphorylation of c-Met receptor tyrosine kinase and further upregulated downstream phosphorylation of phospho-AKT, ERK1/2, and paxillin in a dose-dependent manner (125 μM to 500 μM). c-Met is an important target in lung cancer, and the pathways responsible for ROS generation together may provide novel therapeutic intervention.

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