Genistein-induced apoptosis is estrogen receptor independent.
To test if a link exists between genistein-induced apoptosis and estrogen signaling we co-treated embryos with genistein and with ICI 182,780, a classical estrogen receptor antagonist .
Since adding ICI 182,780, an ER antagonist, does not rescue the genistein-induced apoptosis and since there is no synergistic effect between genistein and estradiol, we conclude that this apoptotic effect elicited by genistein is estrogen-receptors independent.
Genistein in higher concentration induces apoptosis of rat RPE-J cell. z-VAD-fmk inhibited this type of apoptosis and cleavage of PARP enzyme was demonstrated.
The ability of genistein to inhibit the proliferation and to induce apoptosis of RPE cells could be potentially therapeutic for proliferative vitreoretinopathy.
Ten micromolar genistein inhibited cell proliferation by G(0)/G(1) arrest without inducing apoptosis of the major population.
Also, inhibition of caspase-3, -8, and -9 with pharmacological inhibitors reduced genistein-mediated apoptosis.
To determine the apoptotic pathway induced by genistein in the cervical cancer cells, we assessed activation of caspase-3, -8, and -9 by immunoblotting.
Taken together, these results suggest that genistein could induce apoptosis through both extrinsic and intrinsic pathways in human cervical cancer cells.
Sub-G(1) analysis showed that genistein increased apoptotic cells up to 45% at a concentration of 60 micromol/L in HeLa cells, whereas it produced 21% and 17% apoptotic cells in CaSki and C33A cells, respectively, at the same concentration.
Dantrolene, an inhibitor of Ca release from the endoplasmic reticulum, inhibited genistein-induced activation of calpain and caspase 7, in addition to effectively negating genistein-induced apoptosis.
These results suggest that genistein-induced apoptosis in MCF-7 cells is mediated through calpain-caspase 7 and apoptosis signaling kinase 1-p38 mitogen-activated protein kinase activation cascades that involve Ca release from the endoplasmic reticulum.
The molecular mechanisms of genistein-induced apoptosis of human breast cancer MCF-7 cells were investigated.
It was found that genistein at 100 micromol/l concentration effectively induced apoptosis of MCF-7 cells in 24 h.
Genistein was able to induce apoptosis of transplanted tumor cells.
To investigate genistein-induced apoptosis of implanted tumors of SG7901 cells in nude mice, and the relationship between this apoptosis and expression of Bcl-2 and Bax.
The apoptosis index was increased progressively with increasing genistein dose (28.9% ± 1.2%, 33.8% ± 1.6% and 37.7% ± 1.2%).
Previously, genistein has been shown to inhibit nuclear transcription factor, NF-κB and Akt signaling pathways in cancer cells, leading to apoptosis .
These ELISA results were correlated with those obtained by MTT analysis, suggesting that genistein not only induces cell growth inhibitory activity of SB715992, but also caused induction of apoptotic cell death.
Genistein enhanced pro-apoptotic effect of SB715992
In addition, we also found that genistein could also enhance the induction of apoptosis in PC-3 cells induced by SB715992, suggesting that genistein could be clinically useful when combined with SB715992.
This finding suggests that genistein could sensitize ovarian cancer cells to platinum and other conventional chemotherapeutic agents-induced apoptotic cell death and these results are consistent with our previous findings in other cancer cell lines .
Genistein can also induce both apoptosis and autophagic cell death in ovarian cancer cells ; however the role of genistein in chemo-resistant ovarian cancer cells has not been investigated.
The Cell Death Detection ELISA Kit (Roche, Palo Alto, CA USA) was used for assessing apoptosis in A2780 and C200 cells treated with genistein, cisplatin, taxotere, gemcitabine and their combinations according to the manufacturer's protocol.
Moreover, genistein also potentiated growth inhibition and apoptosis in certain pancreatic cancer cells by inhibiting Akt and NF-κB .
To examine genistein's effect on breast cancer cells with different Bcl-2 levels, we established control (MCF-7/PV) and Bcl-2 overexpressing MCF-7 (MCF-7/Bcl-2) cell lines and characterized genistein regulated apoptosis and cell cycle progression in these cells.
Taken together, our results indicate that genistein-Bcl-2 interaction switches Bcl-2 from an anti-apoptotic protein into a proapoptotic protein, which involves disturbed Bcl-2/Bax distribution in mitochondria, increased cytochrome c release and modified cell cycle regulation.
A second series of experiments were performed to determine the degree of genistein-induced apoptosis in these cells, using Apop-Tag kit reagents, to detect apoptotic cells in situ by specific end labeling, and detection of DNA fragments produced by the apoptotic process.
The results obtained indicate that: i) genistein inhibits the growth and proliferation of testicular cells; ii) growth inhibition and proliferation is dose- and exposure-time dependent; iii) there is significant difference in sensitivity of the different testicular cells to genistein; iv) genistein induces apoptosis in testicular cells in a concentration-dependent manner.
Genistein can affect the ERK5 MAPK signaling transduction pathway and induce the expressions of apoptosis related proteins to inhibit the proliferation of MDA-MB-231 cells.
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