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Targeting the ILK/YAP axis by LFG-500 blocks epithelial–mesenchymal transition and metastasis

  
@article{APS10423,
	author = {Cheng-lin Li and Juan Li and Shu-yuan Gong and Meng Huang and Rui Li and Gui-xiang Xiong and Fan Wang and Qiu-ming Zou and Qi Qi and Xiao-xing Yin},
	title = {Targeting the ILK/YAP axis by LFG-500 blocks epithelial–mesenchymal transition and metastasis},
	journal = {Acta Pharmacologica Sinica},
	volume = {42},
	number = {11},
	year = {2021},
	keywords = {},
	abstract = {Metastasis is the main cause of mortality in patients with cancer. Epithelial–mesenchymal transition (EMT), a crucial process in cancer metastasis, is an established target for antimetastatic drug development. LFG-500, a novel synthetic flavonoid, has been revealed as a potential antitumor agent owing to its various activities, including modulation of EMT in the inflammatory microenvironment. Here, using a transforming growth factor beta (TGF-β)-induced EMT models, we found that LFG-500 inhibited EMT-associated migration and invasion in human breast cancer, MCF-7, and lung adenocarcinoma, A549, cell lines, consistent with the observed downregulation of YAP activity. Further studies demonstrated that LGF-500-induced suppression of YAP activation was mediated by integrin-linked kinase (ILK), suggesting that the ILK/YAP axis might be feasible target for anti-EMT and antimetastatic treatments, which was verified by a correlation analysis with clinical data and tumor specimens. Hence, our data support the use of LGF-500 as an antimetastatic drug in cancer therapy and provide evidence that the ILK/YAP axis is a feasible biomarker of cancer progression and a promising target for repression of EMT and metastasis in cancer therapy.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/10423}
}