Department of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, 530021, People's Republic of China.
Department of Bone and Soft Tissue Surgery, Guangxi Medical University Cancer Hospital, Nanning, 530021, People's Republic of China.
Biomed Pharmacother. 2020 Jun;126:110096. doi: 10.1016/j.biopha.2020.110096. Epub 2020 Mar 13.
Calycosin is reportedly evidenced with pharmacologically treating bone cells. However, the comprehensive anti-osteosarcoma (OS) mechanisms of calycosin have not been uncovered. By using a systemic method of network pharmacology, the present study aimed to reveal potential anti-OS biotargets and molecular mechanisms played by calycosin. Moreover, human and animal experiments were conducted to verify the core biotargets of calycosin against OS. As results, all primary and core biotargets, biological processes, molecular pathways of calycosin against OS were revealed. Additionally, top 20 biological processes and pathways of calycosin against OS were identified. In human study, the OS sections resulted in reduced expressions of tumor protein p53 (TP53), Caspase-3 (CASP3), and elevated X-linked inhibitor of apoptosis protein (XIAP) expression in comparison with OS-free controls. As shown in cell culture study, calycosin-treated OS cells showed reduced cell proliferation, and promoted cell apoptosis. In TUNEL stains, calycosin resulted in elevated apoptotic cells. As showed in immunostaining, calycosin-treated OS cells exhibited intracellular up-regulation of TP53, CASP3 expressions, and decreased XIAP expressions. Taken together, the biological informational findings manifest the candidate and core biotargets, molecular functions and pathways of calycosin against OS. Attractively, these core biotargets may be used for effectively detecting and treating human OS.
毛蕊异黄酮据称可用于治疗骨细胞。然而，毛蕊异黄酮的全面抗骨肉瘤（OS）机制尚未被揭示。本研究采用系统的网络药理学方法，旨在揭示毛蕊异黄酮潜在的抗 OS 生物靶标和分子机制。此外，还进行了人体和动物实验来验证毛蕊异黄酮对 OS 的核心生物靶标。结果显示，毛蕊异黄酮针对 OS 的所有主要和核心生物靶标、生物过程和分子途径都被揭示出来。此外，还确定了毛蕊异黄酮针对 OS 的前 20 个生物过程和途径。在人体研究中，骨肉瘤部位的肿瘤蛋白 p53（TP53）、半胱天冬酶-3（CASP3）表达减少，凋亡抑制蛋白 X 连锁（XIAP）表达增加，与无骨肉瘤对照组相比。如细胞培养研究所示，毛蕊异黄酮处理的 OS 细胞表现出细胞增殖减少和促进细胞凋亡。在 TUNEL 染色中，毛蕊异黄酮导致凋亡细胞增加。免疫染色显示，毛蕊异黄酮处理的 OS 细胞表现出细胞内 TP53、CASP3 表达上调和 XIAP 表达下调。综上所述，这些生物学信息发现表明了毛蕊异黄酮针对 OS 的候选和核心生物靶标、分子功能和途径。引人注目的是，这些核心生物靶标可用于有效检测和治疗人类 OS。
