Full extract of Euphorbia esula reversed chemoresistance, inhibited cell migration/invasion, and induced apoptosis of multidrug-resistant SGC7901/VCR cells

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Abstract
Pharmacognosy Magazine,2018,14,56,411-417.
Published:August 2018
Type:Original Article
Authors:
Author(s) affiliations:

Xianli Guo1, Xiaodong Han2, Ziwei Tian1, Zhaoying Fu3
1 Department of Biochemistry, College of Medicine, Yanan University, Yan'an, Shaanxi, China
2 Department of Biochemistry, College of Medicine, Yanan University, Yan'an; Rainbow Hospital, Xianyang, Shaanxi, China
3 Rainbow Hospital, Xianyang; Institute of Molecular Biology and Immunology, Yanan University, Yan'an, Shaanxi, China

Abstract:

Background: The plant Euphorbia esula has been used by ancient Chinese people to treat cancer and other ailments and is used by present doctors or folks as an assistant treatment for some kind of cancers, but the mode of action is unclear. Objective: To investigate the influence of E. esula full extract on chemoresistance, cell migration/invasion, and apoptosis of multidrug-resistant human stomach cancer cells. Materials and Methods: After treating multidrug-resistant human stomach cancer SGC7901/VCR cells with E. esula extract at varying concentrations, the inhibition of cell proliferation was detected using thiazolyl blue. Sensitivity to the chemotherapeutic drugs, adriamycin and paclitaxel, was evaluated using half maximal inhibitory concentration. Cell cycle progression was analyzed by flow cytometry. The inhibitions of cell migration and invasion were examined by Transwell method. The induction of apoptosis and the apoptotic rate were studied by electron microscopy and flow cytometry, respectively. Activation of caspase 3 enzyme was inspected by ultraviolet spectrophotometry. Results: E. esula extract could increase the sensitivity of SGC7901/VCR cells to the chemotherapeutic drugs, adriamycin and paclitaxel. The proliferation, migration, and invasion of SGC7901/VCR cells were significantly inhibited by E. esula extract (P < 0.01 compared with negative control), which showed time- and dose-dependent manners (P < 0.05 and P < 0.01, respectively). Cell cycle was arrest at the S phase. E. esula extract also induced apoptosis in SGC7901/VCR cells, and the apoptotic rate was increased significantly with drug concentration and with treatment time (P < 0.01 compared with negative control, P < 0.05 between concentrations and time points). E. esula extract upregulated enzymatic activity of caspase 3. Conclusion: E. esula extract could reverse SGC7901/VCR cell's resistance to chemotherapeutic drugs and could inhibit cell proliferation, migration, and invasion, interfere with cell cycle progression, and induce apoptosis in SGC7901/VCR cells.

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