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Induction of apoptotic death by curcumin in human tongue squamous cell carcinoma SCC-4 cells is mediated through endoplasmic reticulum stress and mitochondria-dependent pathways

Authors :
Chao Lin Kuo
Shan Ying Wu
Jai Sing Yang
Chun Shu Yu
Heng Chien Ho
Hsiung Kwang Chung
Siu Wan Ip
Shang Ming Chiou
Chien Chih Yu
Jing Gung Chung
Zen Pin Lin
Source :
Cell Biochemistry and Function. 29:641-650
Publication Year :
2011
Publisher :
Wiley, 2011.

Abstract

Curcumin from the rhizome of the Curcuma longa plant has been noted for its chemo-preventative and chemo-therapy activities, and it inhibits the growth of many types of human cancer cell lines. In this study, the mechanisms of cell death involved in curcumin-induced growth inhibition, including cell cycle arrest and induction of apoptosis in human tongue cancer SCC-4 cells, were investigated. Herein, we observed that curcumin inhibited cell growth of SCC-4 cells and induced cell death in a dose-dependent manner. Treatment of SCC-4 cells with curcumin caused a moderate and promoted the G(2) /M phase arrest, which was accompanied with decreases in cyclin B/CDK1 and CDC25C protein levels. Moreover, curcumin significantly induced apoptosis of SCC-4 cells with a decrease of the Bcl-2 level, reduction of mitochondrial membrane potential (ΔΨ(m) ), and promoted the active forms of caspase-3. Curcumin also promoted the releases of AIF and Endo G from the mitochondria in SCC-4 cells by using confocal laser microscope. Therefore, we suggest that curcumin induced apoptosis through a mitochondria-dependent pathway in SCC-4 cells. In addition, we also found that curcumin-induced apoptosis of SCC-4 cells was partly through endoplasmic reticulum stress. In conclusion, curcumin increased G(2) /M phase arrest and induced apoptosis through ER stress and mitochondria-dependent pathways in SCC-4 cells.

Details

ISSN :
02636484
Volume :
29
Database :
OpenAIRE
Journal :
Cell Biochemistry and Function
Accession number :
edsair.doi...........f781a0e4e03b5c3f558131cfdea01f9a
Full Text :
https://doi.org/10.1002/cbf.1800