biochanin a modulates cell viability, invasion, and growth promoting signaling pathways in her-2-positive breast cancer cellsbiochanin调节细胞生存能力、入侵和增长促进her-2-positive乳腺癌细胞信号通路.pdfVIP
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biochanin a modulates cell viability, invasion, and growth promoting signaling pathways in her-2-positive breast cancer cellsbiochanin调节细胞生存能力、入侵和增长促进her-2-positive乳腺癌细胞信号通路
Hindawi Publishing Corporation
Journal of Oncology
Volume 2009, Article ID 121458, 10 pages
doi:10.1155/2009/121458
Research Article
Biochanin A Modulates Cell Viability, Invasion, and
Growth Promoting Signaling Pathways in HER-2-Positive
Breast Cancer Cells
Vikas Sehdev, James C. K. Lai, and Alok Bhushan
Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy Idaho, Biomedical Research Institute,
Idaho State University, Pocatello, ID 83209, USA
Correspondence should be addressed to Alok Bhushan, abhushan@
Received 24 June 2009; Revised 3 November 2009; Accepted 10 November 2009
Recommended by Bruno Vincenzi
Overexpression of HER-2 receptor is associated with poor prognosis and aggressive forms of breast cancer. Scientific literature
indicates a preventive role of isoflavones in cancer. Since activation of HER-2 receptor initiates growth-promoting events in cancer
cells, we studied the effect of biochanin A (an isoflavone) on associated signaling events like receptor activation, downstream
signaling, and invasive pathways. HER-2-positive SK-BR-3 breast cancer cells, MCF-10A normal breast epithelial cells, and NIH-
3T3 normal fibroblast cells were treated with biochanin A (2–100 μM) for 72 hours. Subsequently cell viability assay, western
blotting and zymography were carried out. The data indicate that biochanin A inhibits cell viability, signaling pathways, and
invasive enzyme expression and activity in SK-BR-3 cancer cells. Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability.
Therefore, biochanin A could be a unique natural anticancer agent which can selectively target cancer cells and inhibit multiple
signaling pathways in HER-2-positive breast cancer cells.
Copyright © 2009 Vikas Sehdev et al.
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