Mechanisms for 2-methoxyestradiol-induced apoptosis of prostate cancer cells |
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Authors: | Bu Shizhong Blaukat Andree Fu Xin Heldin Nils Erik Landström Maréne |
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Institution: | Ludwig Institute for Cancer Research, Biomedical Center, Box 595, Uppsala, Sweden. |
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Abstract: | Prostate and breast carcinomas are sex hormone-related carcinomas, which are known to be associated with an over-expression of the proto-oncogene Bcl-2. Here, we report that 2-methoxyestradiol (2-ME), an endogenous metabolite of estrogen that does not bind to nuclear estrogen receptors, effectively induces apoptosis in Bcl-2-expressing human prostate and breast carcinoma cells in vitro and in a rat prostate tumor model in vivo. In several cell lines derived from prostate, breast, liver and colorectal carcinomas, 2-ME treatment led to an activation of c-Jun N-terminal kinase (JNK) and phosphorylation of Bcl-2, which preceded the induction of apoptosis. In summary, our data suggest that 2-ME induces apoptosis in epithelial carcinomas by causing phosphorylation of JNK, which appears to be correlated with phosphorylation of Bcl-2. |
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Keywords: | Apoptosis Bcl-2 Breast cancer 2-Methoxyestradiol Prostate cancer Stress-activated protein kinase/c-Jun N-terminal kinase |
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