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: Xuan Wang, Qi-Hui Shao, Hao Zhou, Jun-Lu Wu, Wen-Qiang Quan, Ping Ji, Yi-Wen Yao, Dong Li, Zu-Jun Sun
المصدر: BMC Complementary Medicine and Therapies, Vol 20, Iss 1, Pp 1-11 (2020)
بيانات النشر: BMC, 2020.
سنة النشر: 2020
المجموعة: LCC:Other systems of medicine
مصطلحات موضوعية: Ginkgolide B, Light chain 3B, NLRP3, Beclin-1, Autophagy, Other systems of medicine, RZ201-999
الوصف: Abstract 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.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2662-7671
Relation: http://link.springer.com/article/10.1186/s12906-020-02980-x; https://doaj.org/toc/2662-7671
DOI: 10.1186/s12906-020-02980-x
URL الوصول: https://doaj.org/article/0b562bfdb6744fdd849ba00549f140c5
رقم الأكسشن: edsdoj.0b562bfdb6744fdd849ba00549f140c5
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:26627671
DOI:10.1186/s12906-020-02980-x