Table 1 |
||
|
Summary of the putative anticancer mechanisms of soy and isolated phyto-oestrogen compounds in breast cancer cell lines and rodent models |
||
|
Phyto-oestrogen |
Cellular effect |
Proposed mechanism |
|
|
||
|
Cell culture studies |
||
|
Genistein |
Growth inhibition |
↓EGF receptor activity [23] |
|
Induction of cell differentiation [43] |
||
|
↓AP-1 activity, ↓ERK phosphorylation [58] |
||
|
↑p21WAF1 [59] |
||
|
↑TGF-β synthesis [75] |
||
|
Induction of apoptosis |
↑Bax, ↑p53 [67] |
|
|
Biochanin A |
Growth inhibition |
↓ER |
|
Resveratrol |
Growth inhibition |
↓NF-κB activation [39] |
|
(-)-Epigallocatechin |
Induction of apoptosis |
↓Bcl-2, ↑Bax [70] |
|
Epigallocatechin-3 gallate |
Growth inhibition |
↓Her-2/neu signalling [71] |
|
Rodent models |
||
|
Genistein |
Mammary tumour suppression |
Induction of terminal differentiation [38] |
|
Resveratrol |
Mammary tumour suppression |
↓NF-κB activation [39] |
|
Soy isoflavone extract |
Mammary tumour suppression |
↓ER-α, ↓PR [42] |
|
Isoflavone mix |
Reduced metastases |
|
|
|
||
|
↓ and ↑ indicate a respective reduction or increase in protein levels or activity. AP, activator protein; EGF, epidermal growth factor; ER, oestrogen receptor; ERK, extracellular signal-related kinase; NF-κB, nuclear factor-κB; TGF, transforming growth factor. |
||
|
Limer and Speirs Breast Cancer Res 2004 6:119 doi:10.1186/bcr781 |
||