Abstract Title:

DNA damage and endoplasmic reticulum stress mediated curcumin-induced cell cycle arrest and apoptosis in human lung carcinoma A-549 cells through the activation caspases cascade- and mitochondrial-dependent pathway.

Abstract Source:

Cancer Lett. 2008 Dec 8;272(1):77-90. Epub 2008 Aug 12. PMID: 18701210

Abstract Author(s):

Song-Shei Lin, Hsuan-Pang Huang, Jai-Sing Yang, Jeng-Yuan Wu, Te-Chun Hsia, Te-Chun Hsai, Chin-Chung Lin, Cheng-Wen Lin, Chao-Lin Kuo, W Gibson Wood, Jing-Gung Chung

Article Affiliation:

Department of Radiological Technology, Central Taiwan University of Science and Technology, No. 11, Buzih Lane, Buzih District, Taichung 40605, Taiwan.


Curcumin, a major component of the Curcuma species, is known to have antioxidant, anti-inflammatory properties and induce apoptosis of cancer cells, however, the precise molecular mechanisms of apoptosis in vitro are unclear. In this study, we showed that curcumin, a plant product containing the phenolic phytochemical, caused DNA damage and endoplasmic reticulum (ER) stress and mitochondrial-dependent-induced apoptosis through the activation of caspase-3 at a treatment concentration of 30 microM in human lung cancer A-549 cells. In contrast, treatment with 5-10 microM of curcumin did not induce significant apoptosis, but rather induced G2/M-phase arrest in A-549 cells. Flow cytometric analysis indicated that curcumin directly increased intracellular oxidative stress based on the cell permeable dye, 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) acting as an indicator of reactive oxygen species (ROS) generation. GADD153 and GRP78 were increased by curcumin which was indicative of ER stress. Curcumin increased Ca(2+) levels and the mitochondrial membrane potential (DeltaPsi(m)), was decreased in A-549 cells. Overall, our results demonstrated that curcumin treatment causes cell death by activating pathways inducing G2/M-phase arrest and apoptosis.

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