Suppr超能文献

大麻二酚与 MCF7 细胞中化疗药物的协同作用:相互作用模式及机制的蛋白质组学分析。

Synergistic Interactions of Cannabidiol with Chemotherapeutic Drugs in MCF7 Cells: Mode of Interaction and Proteomics Analysis of Mechanisms.

机构信息

NICM Health Research Institute, Western Sydney University, Penrith, NSW 2747, Australia.

Department of Pharmacognosy, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.

出版信息

Int J Mol Sci. 2021 Sep 18;22(18):10103. doi: 10.3390/ijms221810103.

Abstract

Cannabidiol (CBD), a nonpsychoactive phytocannabinoid, has recently emerged as a potential cytotoxic agent in addition to its ameliorative activity in chemotherapy-associated side effects. In this work, the potential interactions of CBD with docetaxel (DOC), doxorubicin (DOX), paclitaxel (PTX), vinorelbine (VIN), and 7-ethyl-10-hydroxycamptothecin (SN-38) were explored in MCF7 breast adenocarcinoma cells using different synergy quantification models. The apoptotic profiles of MCF7 cells after the treatments were assessed via flow cytometry. The molecular mechanisms of CBD and the most promising combinations were investigated via label-free quantification proteomics. A strong synergy was observed across all synergy models at different molar ratios of CBD in combination with SN-38 and VIN. Intriguingly, synergy was observed for CBD with all chemotherapeutic drugs at a molar ratio of 636:1 in almost all synergy models. However, discording synergy trends warranted the validation of the selected combinations against different models. Enhanced apoptosis was observed for all synergistic CBD combinations compared to monotherapies or negative controls. A shotgun proteomics study highlighted 121 dysregulated proteins in CBD-treated MCF7 cells compared to the negative controls. We reported the inhibition of topoisomerase II β and α, cullin 1, V-type proton ATPase, and CDK-6 in CBD-treated MCF7 cells for the first time as additional cytotoxic mechanisms of CBD, alongside sabotaged energy production and reduced mitochondrial translation. We observed 91 significantly dysregulated proteins in MCF7 cells treated with the synergistic combination of CBD with SN-38 (CSN-38), compared to the monotherapies. Regulation of telomerase, cell cycle, topoisomerase I, EGFR1, protein metabolism, TP53 regulation of DNA repair, death receptor signalling, and RHO GTPase signalling pathways contributed to the proteome-wide synergistic molecular mechanisms of CSN-38. In conclusion, we identified significant synergistic interactions between CBD and the five important chemotherapeutic drugs and the key molecular pathways of CBD and its synergistic combination with SN-38 in MCF7 cells. Further in vivo and clinical studies are warranted to evaluate the implementation of CBD-based synergistic adjuvant therapies for breast cancer.

摘要

大麻二酚(CBD)是一种非精神活性植物大麻素,除了在化疗相关副作用方面具有改善作用外,最近还被发现具有潜在的细胞毒性。在这项工作中,使用不同的协同作用定量模型,在 MCF7 乳腺癌腺癌细胞中探索了 CBD 与多西他赛(DOC)、阿霉素(DOX)、紫杉醇(PTX)、长春瑞滨(VIN)和 7-乙基-10-羟基喜树碱(SN-38)的潜在相互作用。通过流式细胞术评估 MCF7 细胞经处理后的凋亡谱。通过无标记定量蛋白质组学研究 CBD 和最有前途的组合的分子机制。在不同的 CBD 摩尔比与 SN-38 和 VIN 联合使用的所有协同作用模型中都观察到了强烈的协同作用。有趣的是,在几乎所有的协同作用模型中,CBD 与所有化疗药物在 636:1 的摩尔比下都表现出协同作用。然而,由于协同作用趋势不一致,需要针对不同的模型对选定的组合进行验证。与单药治疗或阴性对照相比,所有协同 CBD 组合均观察到增强的凋亡。一项 shotgun 蛋白质组学研究报告称,与阴性对照相比,CBD 处理的 MCF7 细胞中有 121 个蛋白失调。我们首次报道 CBD 处理的 MCF7 细胞中拓扑异构酶 IIβ和α、Cullin1、V 型质子 ATP 酶和 CDK-6 的抑制作用,以及能量产生受阻和线粒体翻译减少,作为 CBD 的附加细胞毒性机制。与单药治疗相比,用 CBD 与 SN-38(CSN-38)协同治疗的 MCF7 细胞中有 91 个蛋白显著失调。调节端粒酶、细胞周期、拓扑异构酶 I、EGFR1、蛋白质代谢、TP53 对 DNA 修复的调节、死亡受体信号转导和 RHO GTPase 信号通路对 CSN-38 的全蛋白质协同分子机制有贡献。总之,我们在 MCF7 细胞中鉴定了 CBD 与五种重要化疗药物之间的显著协同相互作用,以及 CBD 及其与 SN-38 的协同组合的关键分子途径。需要进一步的体内和临床研究来评估基于 CBD 的协同辅助治疗在乳腺癌中的应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4ee2/8469885/6988a807573b/ijms-22-10103-g001.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验