PI3K/AKT/mTOR通路
蛋白激酶B
上皮-间质转换
信号转导
癌症研究
纤维连接蛋白
化学
波形蛋白
罗亚
细胞生物学
鱼腥草素骨
细胞迁移
生物
细胞
下调和上调
生物化学
免疫学
基因
免疫组织化学
骨钙素
碱性磷酸酶
酶
作者
Yumeng Wang,Yixia Zhang,Yonghui Li,Xiaohong Kou,Zhaohui Xue
标识
DOI:10.1021/acs.jnatprod.2c00457
摘要
Epithelial-mesenchymal transition (EMT) is an important step in tumor progression, which enables tumor cells to acquire migration and invasion characteristics. The aim of this study was to investigate the mechanism of biological biochanin A (BCA) in ameliorating fine particulate matter (PM2.5) lung injury. The results showed that PM2.5 could induce spindle-like changes in cell morphology, causing the ability of migration and invasion. However, they were significantly inhibited by BCA treatment (10/20/30 μm). After BCA treatment, the release and transcription of chemokine CXCL12 and its receptor gene CXCR4 were inhibited, and the release of growth inducer TGF-β1 was significantly reduced. In addition, BCA promoted the transcription of E-cadherin and β-catenin, inhibiting the expression of N-cadherin, vimentin, and fibronectin, and down-regulated the expression of MMP-2/9. We found that BCA effectively interfered with the PI3K/Akt signaling pathway activated by PM2.5. In conclusion, PM2.5 can induce EMT in lung cancer cells, and BCA may reverse this process by activating the PI3K/Akt signaling pathway.
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