细胞周期蛋白D1
细胞凋亡
车站3
骨肉瘤
免疫印迹
细胞周期
信号转导
细胞生长
癌症研究
原癌基因酪氨酸蛋白激酶Src
生物
细胞周期检查点
化学
细胞生物学
生物化学
基因
作者
Liru Tian,Chuan Li,Limin Xiang,Jia Zeng,Shuqing Chen,Weimin Guo,Shulin Chen,Yihai Wang,Xiangjiu He,Peiqiang Su,Caixia Xu
出处
期刊:Phytomedicine
[Elsevier]
日期:2023-04-03
卷期号:114: 154799-154799
被引量:1
标识
DOI:10.1016/j.phymed.2023.154799
摘要
T52 is a steroidal saponin extracted from the traditional Chinese herb Rohdea fargesii (Baill.), and it is reported to possess strong anti-proliferative capabilities in human pharyngeal carcinoma cell lines. However, whether T52 has anti-osteosarcoma properties, and its potential mechanism is remains unknown. To examine the outcome and underlying mechanism of T52 in osteosarcomas (OS). The physiological roles of T52 in OS cells were examined using CCK-8, colony formation (CF), EdU staining, cell cycle/apoptosis and cell migration/invasion assays. The relevant T52 targets against OS were assessed via bioinformatics prediction, and the binding sites were analyzed by molecular docking. Western blot analysis was carried out to examine the levels of factors associated with apoptosis, cell cycle, and STAT3 signaling pathway activation. T52 markedly diminished the proliferation, migration, and invasion of OS cells, and promoted G2/M arrest and apoptosis in a dose-dependent fashion (DDF) in vitro. Mechanistically, molecular docking predicted that T52 stably associated with STAT3 Src homology 2 (SH2) domain residues. Western blot revealed that T52 suppressed the STAT3 signaling pathway, as well as the expression of the downstream targets, such as, Bcl-2, Cyclin D1, and c-Myc. In addition, the anti-OS property of T52 were partially reversed by STAT3 reactivation, which confirmed that STAT3 signaling is critical for regulating the anti-OS property of T52. We firstly demonstrated that T52 possessed strong anti-osteosarcoma property in vitro, which was brought on by the inhibition of the STAT3 signaling pathway. Our findings provided pharmacological support for treating OS with T52.
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