Mechanisms of Biochanin A Alleviating PM2.5 Organic Extracts-Induced EMT of A549 Cells through the PI3K/Akt Pathway

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...

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Veröffentlicht in:Journal of natural products (Washington, D.C.) D.C.), 2022-10, Vol.85 (10), p.2290-2301
Hauptverfasser: Wang, Yumeng, Zhang, Yixia, Li, Yonghui, Kou, Xiaohong, Xue, Zhaohui
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container_issue 10
container_start_page 2290
container_title Journal of natural products (Washington, D.C.)
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creator Wang, Yumeng
Zhang, Yixia
Li, Yonghui
Kou, Xiaohong
Xue, Zhaohui
description 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.
doi_str_mv 10.1021/acs.jnatprod.2c00457
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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. 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Nat. Prod</addtitle><date>2022-10-28</date><risdate>2022</risdate><volume>85</volume><issue>10</issue><spage>2290</spage><epage>2301</epage><pages>2290-2301</pages><issn>0163-3864</issn><eissn>1520-6025</eissn><abstract>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. 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