Biochanin A extirpates the epithelial-mesenchymal transition in a human lung cancer.

The natural iso-flavonoid, biochanin A, is categorized as a phytoestrogen and has been demonstrated to exhibit various pharmacological properties. However, no effects of biochanin A on lung cancer cell lines have been reported. Therefore, the present study aimed to demonstrate whether biochanin A has the ability to reduce lung cancer triggered pro-inflammatory effects from leukemic monocytes. We studied the release of cytokines, tumor necrosis factor (TNF)-α and interleukin (IL)-6, from the cocultured cells of A427:AML-193. In addition to this, epithelial-mesenchymal transition was also monitored. In the cocultured A427 and AML-193, AML-193 was stimulated by A427 cells assisting the release of TNF-α and IL-6 cytokines, but the addition of A427 with biochanin A reduced A427-triggered generation of cytokines by AML-193. Moreover, this non-functional A427:AML-193 coculture reduced the metastasis effects of A427 cells, as determined by wound healing assays and migration/invasion assays. These results were further confirmed by a reduction in Snail and E-cadherin expression levels, which are indicators of the epithelial-mesenchymal transition. These findings suggest the therapeutic effect of biochanin A against lung cancer evoked inflammation and pro-inflammatory functions from monocytic cells.