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논문 기본 정보

자료유형
학술저널
저자정보
저널정보
대한의생명과학회 대한의생명과학회지 대한의생명과학회지 제11권 제2호
발행연도
2005.6
수록면
175 - 183 (9page)

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The two major isoflavones in soy, genistein and daidzein, are well known to prevent hormone-dependent cancers by their antiestrogenic activity. The exact molecular mechanisms for the protective action are, however, not provided yet. It has been reported that genistein and daidzein have a potential anticancer activity through their antiproliferative effect in many hormone-dependent cancer cell lines. Transforming growth factor-β1 (TGF-β1) has also been found to have cell growth inhibitory effect, especially in mammary epithelial cells. This knowledge led to a hypothetical mechanism that the soy isoflavones-induced growth inhibitory effect can be derived from the regulation of TGF-β1 and TGF-β receptors. In order to test this hypothesis, the effects of the soy isoflavones at various concentrations and periods on the expression of TGF-β1 and TGF-β receptors were investigated by using Northern blot analysis in human breast carcinoma epithelial cell lines, an estrogen receptor positive cell line (MCF-7) and an estrogen receptor negative cell line (MDA-MB-231). As a result, only genistein has shown a profound dose-dependent effect on TGF-β1 expression in the ER<sup>+</sup> cell line within the range of doses tested, and the expression levels are correspondent to their inhibitory activities of cell growth. Moreover, daidzein showed down-regulated TGF-β1 expression at a low dose, the cell growth proliferation was promoted at the same condition. Therefore, antiproliferative activity of the soy isoflavones can be mediated by TGF-β1 expression, and the effects are mainly, if not all, occurred by ER dependent pathway. The expression of TGF-β receptors was induced at a lower dose than the one for TGF-β1 induction regardless of the presence of ER, and the expression patterns are similar to those of the cell growth inhibition. These results indicated that the regulation of TGF-β receptor expression as well, prior to TGF-β1 expression, may be involved in the antiproliferative activity of soy isoflavones. Little or no expression of TGF-β receptors was found in the MCF-7 and MDA-MB-231 cells, suggesting refractory properties of the cells to growth inhibitory effect of the TGF-β1. The soy isoflavones can seemingly restore the sensitivity of growth inhibitory responses to TGF-β1 by re-inducing TGF-β receptors expression. In conclusions, our findings presented in this study show that the antitumorigenic activity of the soy isoflavones could be mediated by not only TGF-β1 induction but TGF-β receptor restoration. Thus, soy isoflavones could be good model molecules to develop new nonsteroidal antiestrogenic chemopreventive agents, associated with, regulation of TGF-β and its receptors.

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