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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Journal of Environmental Pathology, Toxicology and Oncology
Импакт фактор: 1.241 5-летний Импакт фактор: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Печать: 0731-8898
ISSN Онлайн: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2019029196
pages 217-227

Atractylenolide III Enhances the Anti-Neoplastic Efficacy of Docetaxel in Gastric Cancer Cell by Inhibiting Fibroblast Growth Factor Receptors 1, -2, and -4 Expression

Yanxia Ji
Department of Oncology, Handan Central Hospital, Handan 056000, Hebei Province, China
Zhenqiao Kang
Department of Oncology, Handan Central Hospital, Handan 056000, Hebei Province, China
Ning Kang
Department of Clinical Medicine, Hebei North University, Zhangjiakou 075000, Hebei Province, China
Yanzheng Zhao
Department of Oncology, Handan Central Hospital, Handan 056000, Hebei Province, China
Qing Guo
Department of Oncology, Handan Central Hospital, Handan 056000, Hebei Province, China
Yongge Chen
Department of Oncology, Handan Central Hospital, Handan 056000, Hebei Province, China

Краткое описание

Background: Natural active components have been reported to serve as adjuvant medications in the clinical practice of cancer therapeutics. However, the antineoplastic roles of atractylenolide III (ATL) are rarely reported. In the present study, we assessed the functions of ATL combined with docetaxel in gastric cancer cells. Methods: Cell viability and cytotoxic activity were evaluated using CCK-8 and LDH-based cytotoxicity assays, respectively. Protein expression levels were measured by western blotting analysis. Annexin V-FITC/PI staining was used to evaluate cell apoptosis using flow cytometry. Results: AGS and SGC-7901 cell viability was significantly inhibited in ATL combined with docetaxel group compared with docetaxel treatment alone. The levels of LDH, apoptosis rate, and the ratio of BAX to Bcl-2 were significantly elevated in combination treatment group compared to docetaxel treatment alone. Intriguingly, docetaxel combined with ATL resulted in a significant decrease in FGFR1, FGFR2, and FGFR4 protein expression compared with docetaxel treatment alone. Knockout of FGFR1, -2, and -4 exhibited a similar role of medications to inhibit growth and induce apoptosis in AGS and SGC-7901 cells. Conclusions: ATL and docetaxel treatment performed the synergistic effects on the inhibition of growth and induction of apoptosis in gastric cancer cells, and the underlying mechanism was mediated, at least partially, through the inhibition of FGFR1, -2, and -4.

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