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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jul 19, 2008 at 9:37 PM
Subject: Inhibition of Insulin-like Growth Factor 1 Receptor Signaling Enhanced Silibinin-Induced Activation of Death Receptor and Mitochondrial Apoptotic Pathways in Human Breast Cancer MCF-7 Cells.
To: mesothelioma77@gmail.com
[1]J Pharmacol Sci. 2008 Jul; 107(3): 260-9
Wang HJ, Tashiro S, Onodera S, Ikejima T
Silibinin, which had been used as a hepatoprotectant, was shown to have anticancer activity. In this study we investigated the mechanisms of silibinin-induced apoptosis in human breast cancer MCF-7 cells. Expressions of Fas ligand (FasL), Fas-associated death domain protein (FADD), and Bax were significantly up-regulated in silibinin-treated cells, whilst silibinin induced a conspicuous translocation of Bax to mitochondria and release of cytochrome c to the cytosol. Therefore, both the extrinsic Fas death receptor and intrinsic mitochondrial death pathways played essential roles in silibinin-induced apoptosis. It was also found that silibinin markedly decreased protein expression of SIRT1, a mammalian homologue of yeast Sir2, which was proved to have a role in sequestering Bax away from mitochondria. Insulin-like growth factor 1 receptor (IGF-1R), a receptor tyrosine kinase with a crucial role in malignancy development, is expressed in most human primary breast carcinomas. Our results showed that silibinin-induced apoptosis was significantly reinforced by blocking IGF-1R signaling with tyrphostin AG1024, a specific inhibitor of IGF-1R autophosphorylation. Up-regulation of FADD, down-regulation of SIRT1 expression, and activation of the mitochondrial death pathway were apparently enhanced by AG1024 in the silibinin-treated MCF-7 cells.
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Source: http://www.hubmed.org/display.cgi?uids=18635919
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From: HubMed - breast cancer <rssfwd@rssfwd.com>
Date: Sat, Jul 19, 2008 at 9:37 PM
Subject: Inhibition of Insulin-like Growth Factor 1 Receptor Signaling Enhanced Silibinin-Induced Activation of Death Receptor and Mitochondrial Apoptotic Pathways in Human Breast Cancer MCF-7 Cells.
To: mesothelioma77@gmail.com
[1]J Pharmacol Sci. 2008 Jul; 107(3): 260-9
Wang HJ, Tashiro S, Onodera S, Ikejima T
Silibinin, which had been used as a hepatoprotectant, was shown to have anticancer activity. In this study we investigated the mechanisms of silibinin-induced apoptosis in human breast cancer MCF-7 cells. Expressions of Fas ligand (FasL), Fas-associated death domain protein (FADD), and Bax were significantly up-regulated in silibinin-treated cells, whilst silibinin induced a conspicuous translocation of Bax to mitochondria and release of cytochrome c to the cytosol. Therefore, both the extrinsic Fas death receptor and intrinsic mitochondrial death pathways played essential roles in silibinin-induced apoptosis. It was also found that silibinin markedly decreased protein expression of SIRT1, a mammalian homologue of yeast Sir2, which was proved to have a role in sequestering Bax away from mitochondria. Insulin-like growth factor 1 receptor (IGF-1R), a receptor tyrosine kinase with a crucial role in malignancy development, is expressed in most human primary breast carcinomas. Our results showed that silibinin-induced apoptosis was significantly reinforced by blocking IGF-1R signaling with tyrphostin AG1024, a specific inhibitor of IGF-1R autophosphorylation. Up-regulation of FADD, down-regulation of SIRT1 expression, and activation of the mitochondrial death pathway were apparently enhanced by AG1024 in the silibinin-treated MCF-7 cells.
___
Source: http://www.hubmed.org/display.cgi?uids=18635919
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