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Curcumin co-treatment ameliorates resistance to gefitinib in drug-resistant NCI-H1975 lung cancer cells
Authors:Jin Xin  Wang Jue  Shen Huifen  Ran Ran  Xu Kai  Tong Xiangming  Zhang Weiping  Feng Li
Institution:1. Institute of Hematology, the First Affiliated Hospital of Medical School of Zhejiang University, Hangzhou 310003, China;2. Department of Oncology, the Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310005, China;3. Institute of Hematology, Zhejiang Provincial People''s Hospital, Hangzhou 310014, China;4. Traditional Chinese Medicine Department of National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
Abstract:

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.
Keywords:Lung neoplasms  Cell line  tumor  Curcumin  Cell proliferation  Apoptosis  Receptor  epidermal growth factor  Gefitinib
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