Curcumin modulates eukaryotic initiation factors in human lung adenocarcinoma epithelial cells |
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Authors: | Lixia Chen Guoqing Tian Changxia Shao Everardo Cobos Weimin Gao |
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Institution: | (1) Department of Environmental Toxicology and The Institute of Environmental and Human Health (TIEHH), Texas Tech University, Lubbock, TX 79409, USA;(2) Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing, China;(3) Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX, USA; |
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Abstract: | Curcumin, a polyphenolic compound, is the active component of Curcuma longa and has been extensively investigated as an anticancer drug that modulates multiple pathways. Eukaryotic initiation factors
(eIFs) have been known to play important roles in translation initiation, which controls cell growth and proliferation. Little
is known about the effects of curcumin on eIFs in lung cancer. The objective of this study was to exam the curcumin cytotoxic
effect and modulation of two major rate-limiting translation initiation factors, including eIF2α and eIF4E protein expression
levels in lung adenocarcinoma epithelial cell line A549. Cytotoxicity was measured by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium
bromide) assay and protein changes were determined by Western blot. A549 cells were treated with 0–240 μM curcumin for 4–96 h.
The inhibitory effects of curcumin on cytotoxicity were dose- and time-dependent (P < 0.001). The 50% inhibitory curcumin concentrations (IC50s) at 24, 48, 72, and 96 h were 93, 65, 40, and 24 μM, respectively.
Protein expressions of eIF2α, eIF4E, Phospho-4E-BP1 were down-regulated, while Phospho-eIF2α and Phospho-eIF4E were up-regulated
after A549 cells were treated with 20 and 40 μM curcumin for 24 h. In addition, the effects of curcumin on these protein expression
changes followed a significant dose-response (P < 0.05, trend test). These findings suggest that curcumin could reduce cell viability through prohibiting the initiation
of protein synthesis by modulating eIF2α and eIF4E. |
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