Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy
| العنوان: | Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy |
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| المؤلفون: | Qi-Hui Shao, Zujun Sun, Yiwen Yao, Hao Zhou, Xuan Wang, Junlu Wu, Ping Ji, Wenqiang Quan, Dong Li |
| المصدر: | BMC Complementary Medicine and Therapies BMC Complementary Medicine and Therapies, Vol 20, Iss 1, Pp 1-11 (2020) |
| سنة النشر: | 2020 |
| مصطلحات موضوعية: | 0301 basic medicine, Programmed cell death, Lung Neoplasms, Apoptosis, Flow cytometry, 03 medical and health sciences, Lactones, 0302 clinical medicine, Western blot, NLRP3, medicine, Autophagy, Humans, Light chain 3B, Lung cancer, Cell Proliferation, medicine.diagnostic_test, Molecular Structure, Cell growth, Chemistry, Inflammasome, lcsh:Other systems of medicine, lcsh:RZ201-999, medicine.disease, Ginkgolide B, Antineoplastic Agents, Phytogenic, Plant Leaves, 030104 developmental biology, Ginkgolides, Complementary and alternative medicine, A549 Cells, 030220 oncology & carcinogenesis, Cancer research, Beclin-1, medicine.drug, Research Article |
| الوصف: | 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. |
| تدمد: | 2662-7671 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5b699719de4db53189bdd2d25e972e68 https://pubmed.ncbi.nlm.nih.gov/32576183 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....5b699719de4db53189bdd2d25e972e68 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 26627671 |
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