Abstract |
Curcumin ( diferuloylmethane), an active component of the spice turmeric, induces apoptosis in several types of malignancies. However, little is known about its anticancer activity in small cell lung cancer (SCLC). SCLC represents a highly malignant and particularly aggressive form of cancer, with early and widespread metastases and a poor prognosis. In this study, we found that curcumin does not activate caspase-8 cleavage or alter the expression of apoptotic receptors FAS and TRAIL in NCI-H446 cells, suggesting that curcumin-induced apoptosis is not associated with death receptor-mediated pathways in these cells. Instead, curcumin caused apoptosis by increasing Bax expression while decreasing the expression of Bcl-2 and Bcl-xL. Curcumin induced a rapid decrease in mitochondrial membrane potential and the release of cytochrome c into the cytosol, followed by activation of caspase-9 and caspase-3. In addition, curcumin-induced apoptosis was accompanied by an increase of intracellular reactive oxygen species (ROS) level. These results indicated that a ROS-mediated mitochondrial pathway played an important role in the process of curcumin-induced apoptosis of human SCLC NCI-H446 cells.
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Authors | Cheng-Liang Yang, Ye-Gang Ma, Yi-Xue Xue, Yong-Yu Liu, Hui Xie, Guang-Rong Qiu |
Journal | DNA and cell biology
(DNA Cell Biol)
Vol. 31
Issue 2
Pg. 139-50
(Feb 2012)
ISSN: 1557-7430 [Electronic] United States |
PMID | 21711158
(Publication Type: Journal Article)
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Chemical References |
- Antineoplastic Agents, Phytogenic
- Reactive Oxygen Species
- Receptors, Death Domain
- Curcumin
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Topics |
- Antineoplastic Agents, Phytogenic
(pharmacology)
- Apoptosis
(drug effects, physiology)
- Cell Line, Tumor
- Curcumin
(pharmacology)
- Dose-Response Relationship, Drug
- Drug Evaluation, Preclinical
- Humans
- Lung Neoplasms
(pathology)
- Membrane Potential, Mitochondrial
(drug effects, physiology)
- Microscopy, Electron, Transmission
- Mitochondria
(drug effects, metabolism, physiology)
- Reactive Oxygen Species
(metabolism, pharmacology)
- Receptors, Death Domain
(metabolism, physiology)
- Signal Transduction
(drug effects, physiology)
- Small Cell Lung Carcinoma
(pathology)
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