Tri-chalcone suppressed breast cancer cell proliferation and induced apoptosis through intrinsic and extrinsic pathways
Naunyn-Schmiedeberg's Archives of Pharmacology(2024)
摘要
Breast cancer development depends critically on antiproliferative and apoptotic mechanisms. However, the mechanisms underlying the antiproliferative and apoptosis effects of breast cancer treated with tri-chalcone remain unclear. Tri-chalcones have been demonstrated in prior studies to inhibit the proliferation of breast cancer cells (MCF-7). Following the discovery, this study seeks to investigate the effect of tri-chalcone compounds on targets involved in antiproliferative and apoptosis mechanisms. In this study, we employed bioinformatics analysis along with in vitro evaluation using tri-chalcone-treated MCF-7 cells to determine the responses of antiproliferative and apoptosis mechanisms. The analysis revealed that the compounds interact with six apoptosis target receptors: TNFα, Bak, Bcl-2, caspase-9, and caspase-8. Tri-chalcone S1-2 exhibited the strongest binding affinities for TNFα (−7.39 kcal/mol), caspase-8 (−8.43 kcal/mol), caspase-9 (−8.53 kcal/mol), Bcl-2 (−8.51 kcal/mol), and Bak (−7.15 kcal/mol). The tri-chalcone S1-2 paired with the corresponding proteins showed minor flexibility and extremely small changes of less than 0.25 nm during the MD simulation. Additionally, tri-chalcone S1-2 had a significant inhibitory effect on the proliferation of MCF-7 cells (5.31 ± 0.26 µg/mL) compared to other compounds. S1-2 also induced apoptosis, affecting nearly half (43.80
更多查看译文
关键词
Tri-chalcone,Apoptosis,Antiproliferative,Molecular docking,Molecular dynamics simulation,Gene expression
AI 理解论文
溯源树
样例
![](https://originalfileserver.aminer.cn/sys/aminer/pubs/mrt_preview.jpeg)
生成溯源树,研究论文发展脉络
Chat Paper
正在生成论文摘要