Anti-metastatic action of anacardic acid targets VEGF-induced signalling pathways in epithelial to mesenchymal transition
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- Shilpa Puttananjaiah
- Department of Studies in Biotechnology, University of Mysore
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- Kaveri Keshavaiah
- Department of Studies in Biotechnology, University of Mysore Maharani’s PU College
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- Salimath Bharathi P
- Department of Studies in Biotechnology, University of Mysore Petit Institute for Bioengineering and Bioscience, Georgia Institute of Technology
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抄録
Anacardic acid is a major constituent of nutshell of cashew. In this study, we have isolated it from the leaves of Anacardium Occidentale L. using polarity-based fractionation and confirmed the structure using GC-MS, NMR and FT-IR. The main focus of this study is to harness the molecular mechanism of anti-metastatic action of anacardic acid (A1). We have used MCF-7, a weak metastatic and U-87, a highly metastatic, breast and glioma cell lines respectively, for our study. We have shown that VEGF increases migration and invasion activities of MCF-7 cells, upon overexpression of Twist and Snail genes. It is observed from the current study that exposure of MCF-7 cells to A1 resulted in upregulation of epithelial marker E-cadherin with a concomitant decrease in the expression of mesenchymal markers Twist and Snail gene expression besides exhibiting a strong anti-migratory and anti-invasive activity. In metastatic U-87 glioma cells, treatment with A1 decreased the phosphorylation of MAP kinases, inhibited the translocation of Sp1 and down regulated VEGF and Flt-1 gene expression. Overall, the current findings demonstrate for the first time that anacardic acid functions as a potent EMT inhibitor by targeting VEGF signaling pathway, providing a novel template for drug discovery.
収録刊行物
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- Drug Discoveries & Therapeutics
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Drug Discoveries & Therapeutics 9 (1), 53-65, 2015
特定非営利活動法人 バイオ＆ソーシャル・サイエンス推進国際研究交流会