Abstract
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.
Highlights
Breast cancer is the most frequently diagnosed and secondmost morbid form of cancer afflicting women in the USA. [1]
Since the SK-BR-3 breast cancer cells overexpress HER2 receptor protein and lack ER and PR, we used SK-BR3 breast cancer cell line to study the effect of biochanin A on HER-2/ER- subtype of breast cancer [41]
In this study we determined the effect of biochanin A on cell viability, signaling, and invasive pathways in SK-BR-3 breast cancer cells
Summary
Breast cancer is the most frequently diagnosed and secondmost morbid form of cancer afflicting women in the USA. [1]. Breast cancer is a heterogeneous disease with various subtypes exhibiting differential susceptibility to anticancer drugs. Therapy targeting the specific breast cancer subtype is recommended for effective treatment [2, 3]. During the normal course of cellular life-cycle cells grow, differentiate, and die. These three fundamental stages of the cellular life-cycle are highly regulated in normal cells whereas uncontrolled growth, dedifferentiated morphology, and resistance to death are the hallmarks of cancer cells [4, 5]. Breast cancer cells exhibit deregulated signaling pathways that promote uncontrolled growth, impart resistance to cell death, and induce invasion into the surrounding tissues [6]
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