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Article Publish Status: FREE
Abstract Title:

A Mixture of Baicalein, Wogonin, and Oroxylin-A Inhibits EMT in the A549 Cell Linethe PI3K/AKT-TWIST1-Glycolysis Pathway.

Abstract Source:

Front Pharmacol. 2021 ;12:821485. Epub 2022 Feb 9. PMID: 35222014

Abstract Author(s):

Hui-Juan Cao, Wei Zhou, Xiao-Le Xian, Shu-Jun Sun, Pei-Jie Ding, Chun-Yu Tian, Fu-Ling Tian, Chun-Hua Jiang, Ting-Ting Fu, Shu Zhao, Jian-Ye Dai

Article Affiliation:

Hui-Juan Cao

Abstract:

Non-small cell lung cancer (NSCLC) is a worldwide disease with a high morbidity and mortality rate, which is most derived from its metastasis. Some studies show that the epithelial-mesenchymal transition (EMT) process promotes lung cancer cell migration and invasion, leading to NSCLC metastasis. Total flavonoid aglycones extract (TFAE) isolated fromwas reported to inhibit tumor growth and induce apoptosis. In this study, we found that baicalein, wogonin, and oroxylin-A were the active compounds of TFAE. After reconstructing with these three compounds [baicalein (65.8%), wogonin (21.2%), and oroxylin-A (13.0%)], the reconstructed TFAE (reTFAE) inhibited the EMT process of A549 cells. Then, bioinformatic technology was employed to elucidate the potential pharmacodynamic mechanism network of reTFAE. We identified the relationship between reTFAE and PI3K/Akt signaling pathways, with TWIST1 as the key protein. LY294002, the inhibitor of the PI3K/Akt signaling pathway, and knock-down TWIST1 could significantly enhance the efficacy of reTFAE, with increasing expression of epithelial markers and decreasing expression of mesenchymal markers in A549 cells at the same time. Furthermore, stable isotope dimethyl-labeled proteomics technology was conducted to complement the follow-up mechanism that the EMT-inhibition process may be realized through the glycolysis pathway. In conclusion, we claim that TWIST1-targeted flavonoids could provide a new strategy to inhibit EMT progress for the treatment of NSCLC.

Study Type : In Vitro Study

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