دورية أكاديمية

Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy.

التفاصيل البيبلوغرافية
العنوان: Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy.
المؤلفون: Wang, Xuan, Shao, Qi-Hui, Zhou, Hao, Wu, Jun-Lu, Quan, Wen-Qiang, Ji, Ping, Yao, Yi-Wen, Li, Dong, Sun, Zu-Jun
المصدر: BMC Complementary Medicine & Therapies; 6/23/2020, Vol. 20 Issue 1, p1-11, 11p, 4 Diagrams, 4 Graphs
مصطلحات موضوعية: AUTOPHAGY, CELL proliferation, APOPTOSIS, CELL lines, FLOW cytometry, FLUORESCENT antibody technique, GENE expression, HYDROCARBONS, INFLAMMATORY mediators, LUNG tumors, MOLECULAR structure, NERVE tissue proteins, PROTEINS, WESTERN immunoblotting, CYTOMETRY, SIGNAL peptides, PHARMACODYNAMICS
مستخلص: Background: Ginkgolide B (GKB) is a major active component of the extracts of Ginkgo biloba leaves, and it has been used as an anti-cancer agent. However, it is unknown whether GKB has the therapeutic effects on lung cancer. Here, we studied the effects of GKB on lung cancer cells. Methods: The effects of GKB on lung cancer cell proliferation and invasion were analyzed by cell counting kit (CCK-8) and cell invasion assays, respectively. Apoptosis was detected by flow cytometry. Western blot analysis was used to confirm the expression of autophagy-associated proteins in GKB-treated cells. Immunofluorescence analysis was used to analyze the level of light chain 3B (LC3B). Results: Treatment with GKB time-dependently inhibited the proliferation and decreased the invasive capacity of A549 and H1975 cells. GKB induced apoptosis of these cells, but there was no significant effect on apoptosis compared to the control treatment. GKB-induced inhibition of cell proliferation and GKB-induced cell death were due to autophagy rather than apoptosis. GKB-induced autophagy of lung cancer cells was dependent on beclin-1, and autophagy-induced inhibition of the NLRP3 inflammasome contributed to the anti-tumor effect of GKB. Conclusions: GKB-mediated autophagy of lung cancer cells is beclin-1-dependent and results in inhibition of the NLRP3 inflammasome. Therefore, GKB might be a potential therapeutic candidate for the treatment of lung cancer. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:26627671
DOI:10.1186/s12906-020-02980-x