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. 2014 Aug;8(2):454-458.
doi: 10.3892/etm.2014.1771. Epub 2014 Jun 10.

Genistein inhibits the proliferation and differentiation of MCF-7 and 3T3-L1 cells via the regulation of ERα expression and induction of apoptosis (VSports)

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"VSports注册入口" Genistein inhibits the proliferation and differentiation of MCF-7 and 3T3-L1 cells via the regulation of ERα expression and induction of apoptosis

Eun Jeong Choi et al. Exp Ther Med. 2014 Aug.

Abstract

The present study investigated the effect of the phytochemical genistein on the proliferation and differentiation of MCF-7 and 3T3-L1 cells via the regulation of estrogen receptor-α (ERα) expression and the induction of apoptosis. When MCF-7 human breast cancer cells were treated with 50, 100, 150 and 200 μM genistein for 24, 48 or 72 h, cell growth was significantly decreased in a concentration-dependent manner. Notably, the patterns of ERα expression and proliferation in MCF-7 cells treated with genistein were similar. Furthermore, ERα expression in differentiating 3T3-L1 cells was significantly inhibited by 48 h treatment with 50 μM genistein, which was selected based on the results of cytotoxicity assays on 3T3-L1 preadipocytes [lactate dehydrogenase (LDH) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) viability assays]. Under the same conditions, genistein-induced apoptotic features were observed in MCF-7 and differentiating 3T3-L1 cells VSports手机版. This observation is supported by the finding that B-cell lymphoma 2 (Bcl-2) expression was reduced while that of Bcl-2-associated X protein (Bax) was induced by genistein. The results of the present study suggest that an ERα-related pathway and the induction of apoptosis are involved in the proliferation of MCF-7 cells and the differentiation of 3T3-L1 cells. .

Keywords: 3T3-L1 cells; MCF-7 cells; differentiation; estrogen receptor-α; genistein; proliferation V体育安卓版. .

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Figures (VSports)

Figure 1
Figure 1
Antiproliferative effects of genistein on MCF-7 cells. MCF-7 cells were exposed to genistein at 50, 100, 150 and 200 μM for 24, 48 and 72 h. All data are reported as the percentage change, as compared with the control (CTL) group (vehicle only). Values are expressed as mean ± standard deviation. *P<0.05, significantly different from the CTL group.
Figure 2
Figure 2
Cytotoxicity of genistein toward 3T3-L1 preadipocytes. (A) 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. (B) Lactate dehydrogenase (LDH) assay. 3T3-L1 preadipocytes were exposed to genistein at 5, 10, 20, 25, 50 and 100 μM for 24, 48 and 72 h. Values are expressed as means ± standard deviation. *P<0.05, significantly different from the vehicle-only group.
Figure 3
Figure 3
Modulation of estrogen receptor-α (ERα) and cyclin D1 by genistein in MCF-7 and differentiating 3T3-L1 cells. (A) For determination of ERα, MCF-7 cells were exposed to genistein at 50, 100, 150 and 200 μM for 24, 48 and 72 h. (B) In addition, 3T3-L1 and MCF-7 cells were exposed to 50 μM genistein for 48 h. Values are expressed as means ± standard deviations. CTL, control group (vehicle only); *P<0.05, significantly different from the CTL group.
Figure 4
Figure 4
Induction of apoptosis by genistein. Apoptotic changes were detected by (A) 4′,6-diamidino-2-phenyl-indole (DAPI) staining and (B) measurement of the B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein (Bax) ratio. The standard deviations in all the control groups for MCF-7 and 3T3-L1 cells are <0.12. Values are expressed as means ± standard deviations. CTL, control group (vehicle only); *P<0.05, significantly different from the CTL group.

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