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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >A Network Pharmacology Study on the Molecular Mechanisms of FDY003 for Breast Cancer Treatment
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A Network Pharmacology Study on the Molecular Mechanisms of FDY003 for Breast Cancer Treatment

机译:乳腺癌治疗FDY003分子机制的网络药理学研究

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Herbal medicines have drawn considerable attention with regard to their potential applications in breast cancer (BC) treatment, a frequently diagnosed malignant disease, considering their anticancer efficacy with relatively less adverse effects. However, their mechanisms of systemic action have not been understood comprehensively. Based on network pharmacology approaches, we attempted to unveil the mechanisms of FDY003, an herbal drug comprised of Lonicera japonica Thunberg, Artemisia capillaris Thunberg , and Cordyceps militaris , against BC at a systemic level. We found that FDY003 exhibited pharmacological effects on human BC cells. Subsequently, detailed data regarding the biochemical components contained in FDY003 were obtained from comprehensive herbal medicine-related databases, including TCMSP and CancerHSP. By evaluating their pharmacokinetic properties, 18 chemical compounds in FDY003 were shown to be potentially active constituents interacting with 140 BC-associated therapeutic targets to produce the pharmacological activity. Gene ontology enrichment analysis using g:Profiler indicated that the FDY003 targets were involved in the modulation of cellular processes, involving the cell proliferation, cell cycle process, and cell apoptosis. Based on a KEGG pathway enrichment analysis, we further revealed that a variety of oncogenic pathways that play key roles in the pathology of BC were significantly enriched with the therapeutic targets of FDY003; these included PI3K-Akt, MAPK, focal adhesion, FoxO, TNF, and estrogen signaling pathways. Here, we present a network-perspective of the molecular mechanisms via which herbal drugs treat BC.
机译:草药在乳腺癌(BC)治疗中的潜在应用方面具有相当大的关注,经常被诊断的恶性疾病,考虑到它们的抗癌疗效,不良反应。然而,他们的系统行动机制尚未全面地理解。基于网络药理学方法,我们试图揭示FDY003的机制,该机制,该药物由Lonicera japonica Thunberg,Artemisia Capillaris Thunberg和Cordyceps Militaris含有对抗BC的全身水平。我们发现FDY003表现出对人BC细胞的药理学作用。随后,从综合草药相关数据库中获得了关于FDY003中所含的生物化学成分的详细数据,包括TCMSP和CancerHSP。通过评估其药代动力学性质,FDY003中的18个化合物被显示为潜在的活性成分与140bc相关的治疗靶靶相互作用以产生药理活性。使用G的基因本体学富集分析:分析器表明FDY003靶涉及细胞过程的调节,涉及细胞增殖,细胞周期过程和细胞凋亡。基于KEGG途径浓缩分析,我们进一步揭示了在BC病理学中起主要作用的各种致癌途径显着富集了FDY003的治疗靶标;这些包括PI3K-AKT,MAPK,焦粘连,FOXO,TNF和雌激素信号通路。在这里,我们介绍了草药药物治疗BC的分子机制的网络视角。

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