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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

Pathways inhibited by biochanin A in HER-2+ SK-BR-3 breast cancer cells. The protein expression data indicate that biochanin A treatment inhibits growth (p-HER-2, p-Erk), survival (Akt, mTOR, and NFκB), and invasion (MMP-9 and MMP-14) promoting pathways in SK-BR-3 cells.
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fig9: Pathways inhibited by biochanin A in HER-2+ SK-BR-3 breast cancer cells. The protein expression data indicate that biochanin A treatment inhibits growth (p-HER-2, p-Erk), survival (Akt, mTOR, and NFκB), and invasion (MMP-9 and MMP-14) promoting pathways in SK-BR-3 cells.

Mentions: The HER-2-positive subtype of breast cancer has an aggressive malignant phenotype due to HER-2 signaling cascade mediated rapid growth, drug resistance, and distant metastasis. This report indicates that biochanin A, a dietary isoflavone, can inhibit HER-2 receptor activation, downstream signaling pathways (Erk1/2, Akt, and mTOR), and NFκB transcription factor expression. Apart from inhibiting the signaling pathways, biochanin A also inhibits invasive enzyme activity by suppressing MMP-9 protease activity and MT-MMP1 protein expression, respectively. The data (as summarized in Figure 9) suggest that biochanin A is a unique natural compound which selectively targets HER-2+ SK-BR-3 breast cancer cells and inhibits multiple deregulated mechanisms associated with malignant transformation. Therefore, biochanin A should be studied further to determine if it can be used with other conventional chemotherapeutic drugs and/or with HER-2 targeted anticancer drugs for better therapeutic outcome of patients suffering from HER-2/ER-subtype of breast cancer.


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)

Pathways inhibited by biochanin A in HER-2+ SK-BR-3 breast cancer cells. The protein expression data indicate that biochanin A treatment inhibits growth (p-HER-2, p-Erk), survival (Akt, mTOR, and NFκB), and invasion (MMP-9 and MMP-14) promoting pathways in SK-BR-3 cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig9: Pathways inhibited by biochanin A in HER-2+ SK-BR-3 breast cancer cells. The protein expression data indicate that biochanin A treatment inhibits growth (p-HER-2, p-Erk), survival (Akt, mTOR, and NFκB), and invasion (MMP-9 and MMP-14) promoting pathways in SK-BR-3 cells.
Mentions: The HER-2-positive subtype of breast cancer has an aggressive malignant phenotype due to HER-2 signaling cascade mediated rapid growth, drug resistance, and distant metastasis. This report indicates that biochanin A, a dietary isoflavone, can inhibit HER-2 receptor activation, downstream signaling pathways (Erk1/2, Akt, and mTOR), and NFκB transcription factor expression. Apart from inhibiting the signaling pathways, biochanin A also inhibits invasive enzyme activity by suppressing MMP-9 protease activity and MT-MMP1 protein expression, respectively. The data (as summarized in Figure 9) suggest that biochanin A is a unique natural compound which selectively targets HER-2+ SK-BR-3 breast cancer cells and inhibits multiple deregulated mechanisms associated with malignant transformation. Therefore, biochanin A should be studied further to determine if it can be used with other conventional chemotherapeutic drugs and/or with HER-2 targeted anticancer drugs for better therapeutic outcome of patients suffering from HER-2/ER-subtype of breast cancer.

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