Hui Wang1 ,
Wei Qiao2
1Department of Clinical Nutrition;
2Department of Radiology, Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research and The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu 210009, China.
For correspondence:- Hui Wang
Email: tulipglf66@hotmail.com Tel:+862583283598
Accepted: 25 September 2018
Published: 31 October 2018
Citation:
Wang H, Qiao W.
Curcumin induces apoptosis in lung cancer cells via mitochondria-dependent signal pathways. Trop J Pharm Res 2018; 17(10):1933-1938
doi:
10.4314/tjpr.v17i10.6
© 2018 The authors.
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Abstract
Purpose: To investigate the effect of curcumin on the growth and viability of lung cancer cells.
Methods: The viability of curcumin-treated A-427 and A-549 cells, and changes in their morphologies were assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and phase-contrast microscopy, respectively. Flow cytometry and western blot assays were employed for the determination of apoptosis and changes in protein expressions, respectively.
Results: Curcumin treatment altered the morphologies of A-427 and A-549 lung cancer cells. The viability of A-427 cells was reduced to 89, 71, 49, 26 and 25 %, respectively, on treatment with 5, 10, 15, 20 and 25 μM curcumin, while the corresponding decreases in viability of A-549 cells treated with the same doses of curcumin were 91, 74, 53, 31 and 29 %, respectively. Treatment with 20 % curcumin resulted in 62.87 % apoptosis in A-549 lung cancer cells. Curcumin increased the proportion of cells in G0/G1 phase in a concentration-dependent manner, and increased the expressions of p21 and p-p53 proteins in A-427 cells, while the expressions of cyclin E and Cdc25c were decreased. Curcumin treatment also enhanced the expressions of Bax, cleavage-caspase-8 and PARP in A-549 cells.
Conclusion: Curcumin inhibits lung cancer growth by inducing apoptosis and cell cycle arrest. Thus, curcumin has a promising potential for the treatment of lung cancer.
Keywords: Curcumin, Lung cancer, Apoptosis, Viability, Intrinsic, Reactive oxygen species