芹菜素
PI3K/AKT/mTOR通路
蛋白激酶B
癌变
化学
干细胞
癌症研究
同源盒蛋白纳米
计算生物学
信号转导
药理学
生物
细胞生物学
生物化学
诱导多能干细胞
类黄酮
胚胎干细胞
基因
抗氧化剂
作者
Mengdie Ou,Zhicheng Deng,Yonghui Shi,Jianxiong He,Zicong Ye,Ming Guo,Guohua Cheng,Junyan Wu,Li Lv
标识
DOI:10.3389/fphar.2024.1496664
摘要
Apigenin (API), a traditionally sourced flavonoid, is recognized for its anti-neoplastic properties. Despite well-documented effects on tumorigenesis, the detailed therapeutic impact on breast cancer stem cells (BCSCs) and the associated molecular mechanisms are yet to be clarified. The objective of this study is to elucidate the therapeutic effects of API on BCSCs and to uncover its molecular mechanisms through network pharmacology and experimental validation. Interactions of API with candidate targets were examined through target screening, enrichment analysis, construction of protein-protein interaction networks, and molecular docking. MCF-7-derived BCSCs were utilized as a model system to investigate and substantiate the anti-BCSC effects of API and the underlying mechanism. Molecular docking studies have shown that API and TP53 exhibit favorable binding affinity. Compared with the negative control group, API effectively suppressed the expression of BCSC-related proteins such as ALDH1A1, NANOG, EpCAM, and MYC, downregulated p-PI3K and p-AKT, and upregulated p53. This study demonstrates that API can play an anti-BCSC role by regulating the PI3K/AKT/p53 pathway in BCSCs of MCF-7 cells, highlighting its potential as a therapeutic agent for targeting BCSCs.
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