Abstract
Recent population studies provide clues that the use of curcumin may be associated with reduced incidence and improved prognosis of certain cancers. In the present study, we demonstrated that curcumin acted as a growth inhibitor for lung cancer cells. Our results found that curcumin inhibited cell proliferation, which was associated with upregulation of the cyclin-dependent kinase inhibitors, p27 and p21, and downregulation of cyclin D1. In addition, we showed that curcumin induced the expression of forkhead box protein O1 (FOXO1) through activation of extracellular signal-regulated kinase 1/2 signaling. These findings provide evidence for a mechanism that may contribute to the antineoplastic effects of curcumin and justify further work to explore potential roles for activators of FOXO1 in the prevention and treatment of lung cancer.
Publication types
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Research Support, Non-U.S. Gov't
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Retracted Publication
MeSH terms
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Antineoplastic Agents / pharmacology*
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Cell Line, Tumor
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Cell Proliferation / drug effects
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Curcumin / pharmacology*
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Cyclin D1 / genetics
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Cyclin D1 / metabolism
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Cyclin-Dependent Kinase Inhibitor p21 / genetics
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Cyclin-Dependent Kinase Inhibitor p21 / metabolism
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Cyclin-Dependent Kinase Inhibitor p27 / genetics
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Cyclin-Dependent Kinase Inhibitor p27 / metabolism
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Disease Progression
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Dose-Response Relationship, Drug
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Forkhead Box Protein O1
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Forkhead Transcription Factors / genetics*
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Forkhead Transcription Factors / metabolism
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Humans
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Lung Neoplasms / genetics*
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Lung Neoplasms / pathology*
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MAP Kinase Signaling System / drug effects
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Neoplasm Metastasis
Substances
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Antineoplastic Agents
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Cyclin-Dependent Kinase Inhibitor p21
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FOXO1 protein, human
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Forkhead Box Protein O1
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Forkhead Transcription Factors
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Cyclin D1
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Cyclin-Dependent Kinase Inhibitor p27
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Curcumin