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Biochanin A Modulates Cell Viability, Invasion, and Growth Promoting Signaling Pathways in HER-2-Positive Breast Cancer Cells.

Sehdev V, Lai JC, Bhushan A - J Oncol (2010)

Bottom Line: Overexpression of HER-2 receptor is associated with poor prognosis and aggressive forms of breast cancer.Subsequently cell viability assay, western blotting and zymography were carried out.Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy Idaho, Biomedical Research Institute, Idaho State University, Pocatello, ID 83209, USA.

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 muM) 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.

No MeSH data available.


Related in: MedlinePlus

Effect of biochanin A on MCF-10A, NIH-3T3, and SK-BR-3 cell viability. SK-BR-3/NIH-3T3 and MCF-10A cells were seeded at 2000 and 5000 cells/well in a 96-well plate. After 8 hours of cell adhesion period, the cells were treated with biochanin A (2–100 μM) for 72 hours. The data indicate a biphasic effect of biochanin A on SK-BR-3 breast cancer cell viability. Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability. C: control or no treatment; DMSO: vehicle  (Statistical analysis: One-way Anova, n = 3, *P < .05).
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fig1: Effect of biochanin A on MCF-10A, NIH-3T3, and SK-BR-3 cell viability. SK-BR-3/NIH-3T3 and MCF-10A cells were seeded at 2000 and 5000 cells/well in a 96-well plate. After 8 hours of cell adhesion period, the cells were treated with biochanin A (2–100 μM) for 72 hours. The data indicate a biphasic effect of biochanin A on SK-BR-3 breast cancer cell viability. Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability. C: control or no treatment; DMSO: vehicle (Statistical analysis: One-way Anova, n = 3, *P < .05).

Mentions: The cell viability assay data (Figure 1) indicate that treatment of SK-BR-3 breast cancer cells with biochanin A (2–100 μM) has a biphasic effect on cancer cell viability. Treatment with 5–20 μM biochanin A induces increased SK-BR-3 breast cancer cell viability whereas treatment with 50–100 μM biochanin A induces a dose-dependent inhibition of cell viability. In contrast with SK-BR-3 breast cancer cell line, treatment of MCF-10A and NIH-3T3 cell lines with biochanin A (2–100 μM) did not inhibit MCF-10A and NIH-3T3 cell viability (Figure 1).


Biochanin A Modulates Cell Viability, Invasion, and Growth Promoting Signaling Pathways in HER-2-Positive Breast Cancer Cells.

Sehdev V, Lai JC, Bhushan A - J Oncol (2010)

Effect of biochanin A on MCF-10A, NIH-3T3, and SK-BR-3 cell viability. SK-BR-3/NIH-3T3 and MCF-10A cells were seeded at 2000 and 5000 cells/well in a 96-well plate. After 8 hours of cell adhesion period, the cells were treated with biochanin A (2–100 μM) for 72 hours. The data indicate a biphasic effect of biochanin A on SK-BR-3 breast cancer cell viability. Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability. C: control or no treatment; DMSO: vehicle  (Statistical analysis: One-way Anova, n = 3, *P < .05).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2821773&req=5

fig1: Effect of biochanin A on MCF-10A, NIH-3T3, and SK-BR-3 cell viability. SK-BR-3/NIH-3T3 and MCF-10A cells were seeded at 2000 and 5000 cells/well in a 96-well plate. After 8 hours of cell adhesion period, the cells were treated with biochanin A (2–100 μM) for 72 hours. The data indicate a biphasic effect of biochanin A on SK-BR-3 breast cancer cell viability. Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability. C: control or no treatment; DMSO: vehicle (Statistical analysis: One-way Anova, n = 3, *P < .05).
Mentions: The cell viability assay data (Figure 1) indicate that treatment of SK-BR-3 breast cancer cells with biochanin A (2–100 μM) has a biphasic effect on cancer cell viability. Treatment with 5–20 μM biochanin A induces increased SK-BR-3 breast cancer cell viability whereas treatment with 50–100 μM biochanin A induces a dose-dependent inhibition of cell viability. In contrast with SK-BR-3 breast cancer cell line, treatment of MCF-10A and NIH-3T3 cell lines with biochanin A (2–100 μM) did not inhibit MCF-10A and NIH-3T3 cell viability (Figure 1).

Bottom Line: Overexpression of HER-2 receptor is associated with poor prognosis and aggressive forms of breast cancer.Subsequently cell viability assay, western blotting and zymography were carried out.Biochanin A did not inhibit MCF-10A and NIH-3T3 cell viability.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical and Pharmaceutical Sciences, College of Pharmacy Idaho, Biomedical Research Institute, Idaho State University, Pocatello, ID 83209, USA.

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 muM) 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.

No MeSH data available.


Related in: MedlinePlus