Display options
Cite
Jin X, Wang J, Shen H, et al. Curcumin co-treatment ameliorates resistance to gefitinib in drug- resistant NCI-H1975 lung cancer cells. J Tradit Chin Med. 2017;37(3):355-360
Jin, X., Wang, J., Shen, H., Ran, R., Xu, K., Zhang, W., Tong, X., & Feng, L. (2017). Curcumin co-treatment ameliorates resistance to gefitinib in drug- resistant NCI-H1975 lung cancer cells. Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan, 37(3), 355-360.
Jin, Xin, et al. "Curcumin co-treatment ameliorates resistance to gefitinib in drug- resistant NCI-H1975 lung cancer cells." Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan vol. 37,3 (2017): 355-360.
Jin X, Wang J, Shen H, Ran R, Xu K, Zhang W, Tong X, Feng L. Curcumin co-treatment ameliorates resistance to gefitinib in drug- resistant NCI-H1975 lung cancer cells. J Tradit Chin Med. 2017 Jun;37(3):355-360. PMID: 31682378.
Copy Download .nbib Format: NLM
Share it on

J Tradit Chin Med. 2017 Jun;37(3):355-360.

Curcumin co-treatment ameliorates resistance to gefitinib in drug- resistant NCI-H1975 lung cancer cells.

Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan

Xin Jin, Jue Wang, Huifen Shen, Ran Ran, Kai Xu, Weiping Zhang, Xiangming Tong, Li Feng

Affiliations

  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.

PMID: 31682378

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: Apoptosi; Cell line, tumor; Cell proliferation; Curcumin; Gefitinib; Lung neoplasm; Receptor, epidermal growth factor

Publication Types

Grant support