Limits...
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 Akt and p-Akt protein expression. (a) SK-BR-3 breast cancer cells were seeded in a T-75 flask in RPMI-1640 cell culture media (10% FBS). Following 72 hours of treatment with biochanin A (2–50 μM) Akt and p-Akt protein expression was evaluated. The data indicate reduced Akt phosphorylation at 50 μM (10.17 ± 7.89; P < .05) biochanin A. C: control or no treatment; DMSO: vehicle  (Statistical analysis: One-way Anova, n = 3, *P < .05). (b) Representative blot for Akt and p-Akt protein expression.
© Copyright Policy - open-access
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2821773&req=5

fig4: Effect of biochanin A on Akt and p-Akt protein expression. (a) SK-BR-3 breast cancer cells were seeded in a T-75 flask in RPMI-1640 cell culture media (10% FBS). Following 72 hours of treatment with biochanin A (2–50 μM) Akt and p-Akt protein expression was evaluated. The data indicate reduced Akt phosphorylation at 50 μM (10.17 ± 7.89; P < .05) biochanin A. C: control or no treatment; DMSO: vehicle (Statistical analysis: One-way Anova, n = 3, *P < .05). (b) Representative blot for Akt and p-Akt protein expression.

Mentions: The Akt pathway is another major downstream signaling pathway associated with cellular growth and viability [49]. Western blotting data (Figure 4) with Akt specific antibody indicate inhibition of Akt phosphorylation with 50 μM (10.17 ± 7.89; P < .05) biochanin A treatment in SK-BR-3 breast cancer cells.


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 Akt and p-Akt protein expression. (a) SK-BR-3 breast cancer cells were seeded in a T-75 flask in RPMI-1640 cell culture media (10% FBS). Following 72 hours of treatment with biochanin A (2–50 μM) Akt and p-Akt protein expression was evaluated. The data indicate reduced Akt phosphorylation at 50 μM (10.17 ± 7.89; P < .05) biochanin A. C: control or no treatment; DMSO: vehicle  (Statistical analysis: One-way Anova, n = 3, *P < .05). (b) Representative blot for Akt and p-Akt protein expression.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig4: Effect of biochanin A on Akt and p-Akt protein expression. (a) SK-BR-3 breast cancer cells were seeded in a T-75 flask in RPMI-1640 cell culture media (10% FBS). Following 72 hours of treatment with biochanin A (2–50 μM) Akt and p-Akt protein expression was evaluated. The data indicate reduced Akt phosphorylation at 50 μM (10.17 ± 7.89; P < .05) biochanin A. C: control or no treatment; DMSO: vehicle (Statistical analysis: One-way Anova, n = 3, *P < .05). (b) Representative blot for Akt and p-Akt protein expression.
Mentions: The Akt pathway is another major downstream signaling pathway associated with cellular growth and viability [49]. Western blotting data (Figure 4) with Akt specific antibody indicate inhibition of Akt phosphorylation with 50 μM (10.17 ± 7.89; P < .05) biochanin A treatment in SK-BR-3 breast cancer cells.

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