髓系白血病
体外
机制(生物学)
化学
PI3K/AKT/mTOR通路
K562细胞
MAPK/ERK通路
药理学
体外毒理学
白血病
计算生物学
磷酸化
信号转导
癌症研究
生物化学
生物
免疫学
认识论
哲学
作者
Dongping Wang,Hongwen Zhu,Wanwen Ge,Yanqing Sun
标识
DOI:10.1002/cbdv.202500758
摘要
Chronic myeloid leukemia (CML) is a malignant hematological neoplasm. FA-2-b-β, extracted from Agaricus blazei Murrill, has demonstrated antitumor activity against multiple cancer types. Nevertheless, the specific pharmacodynamic components and molecular mechanisms of FA-2-b-β against CML remain to be elucidated. This study aimed to systematically investigate the mechanism of FA-2-b-β against CML through an integrated strategy combining liquid chromatography-tandem mass spectrometry (LC-MS/MS), network pharmacology prediction, and in vitro experimental validation. Using LC-MS/MS profiling, we identified a total of 126 chemical components. Subsequently, network pharmacological analysis screened 45 potentially active components and 129 CML-related overlapping targets. Further pathway enrichment analysis revealed that these candidate targets were predominantly involved in the PI3K/AKT and MAPK pathways. In vitro validation confirmed the suppression of PI3K/AKT phosphorylation in K562 cells. Collectively, this study provides significant insights into the active components and antitumor mechanisms of FA-2-b-β, emphasizing its potential as a promising therapeutic agent for treating CML.
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