ArticleExperimental and therapeutic medicine2018
Biochanin A extirpates the epithelial-mesenchymal transition in a human lung cancer.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- Biochanin A, a Plant Isoflavone, Disrupts Peptidoglycan Biosynthesis by DownregulatingAntibiotics (Basel, Switzerland) · 2026Article
- The therapeutic effect and specific mechanism involved active Chinese medicine component biochaninA in glioma.Frontiers in immunology · 2026Article
- Article
- Chemical and Biological Properties of Biochanin A and Its Pharmaceutical Applications.Pharmaceutics · 2023Review
- Mechanisms Behind the Pharmacological Application of Biochanin-A: A review.F1000Research · 2023Review
- Biochanin A Suppresses Tumor Progression and PD-L1 Expression via Inhibiting ZEB1 Expression in Colorectal Cancer.Journal of oncology · 2022Article
- Flavonoids against non-physiologic inflammation attributed to cancer initiation, development, and progression-3PM pathways.The EPMA journal · 2021Review
- Biochanin A Regulates Cholesterol Metabolism Further Delays the Progression of Nonalcoholic Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Biochanin-A ameliorates pulmonary fibrosis by suppressing the TGF-β mediated EMT, myofibroblasts differentiation and collagen deposition in in vitro and in vivo systems.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2020Article
- Reversal of Multidrug Resistance in Cancer by Multi-Functional Flavonoids.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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