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OBJECTIVE: To examine whether a combinative treatment with curcumin enhances the effects of the epidermal growth factor receptor-tyrosine kinase inhibitor(EGFR-TKI) gefitinib on cell proliferation, clonogenic capacity and apoptosis in the drug-resistant lung cancer cell line NCI-H1975, and further investigate the molecular mechanisms involved.METHODS: NCI-H1975 cells were treated with curcumin and gefitinib alone or in combination, and cell proliferation, clonogenic capacity and apoptosis were examined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay, clone forming experiments, and flow cytometry, respectively, while p38, extracellular regulated protein kinase(ERK)1/2, and protein kinase B(AKT)phosphorylation were examined using Western blotting.RESULTS: Compared with the effects of either agent alone, the combination of curcumin and gefitinib had a stronger suppressive effect on proliferation and the clonogenic capacity(P < 0.05), and showed an increased ability to promote apoptosis(P < 0.05) and reduce p38, ERK1/2, and AKT phosphorylation(P < 0.05).CONCLUSION: Co-treatment of curcumin and gefitinib significantly improves the ability of gefitinib to inhibit cell proliferation, suppress the clonogenic capacity and enhance apoptosis in NCI-H1975 cells,and these effects are possibly mediated via a decrease in phosphorylation of proteins in downstream pathways of the epidermal growth factor receptor.
OBJECTIVE: To examine whether a combination of curcumin enhances the effects of the epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) gefitinib on cell proliferation, clonogenic capacity and apoptosis in the drug-resistant lung cancer cell line NCI-H1975, and further investigate the molecular mechanisms involved.METHODS: NCI-H1975 cells were treated with curcumin and gefitinib alone or in combination, and cell proliferation, clonogenic capacity and apoptosis were examined using the 3- (4,5-dimethylthiazol-2-yl) 2, 5-diphenyltetrazolium bromide (MTT) assay, clone forming experiments, and flow cytometry, respectively, while while p38, extracellular regulated protein kinase (ERK) 1/2, and protein kinase B (AKT) phosphorylation were examined using Western blotting. RESULTS: Compared with the effects of either agent alone, the combination of curcumin and gefitinib had a stronger suppressive effect on proliferation and the clonogenic capacity (P <0.05), and showed an increas Inhibitory to promote apoptosis (P <0.05) and reduce p38, ERK1 / 2, and AKT phosphorylation (P <0.05) .CONCLUSION: Co-treatment of curcumin and gefitinib significantly improves the ability of gefitinib to inhibit cell proliferation, suppress the clonogenic capacity and enhance apoptosis in NCI-H1975 cells, and these effects are possible mediated via a decrease in phosphorylation of proteins in downstream pathways of the epidermal growth factor receptor.