Mechanisms for 2-methoxyestradiol-induced apoptosis of prostate cancer cells
2002 (English)In: FEBS Letters, ISSN 0014-5793, Vol. 531, no 2, 141-51 p.Article in journal (Refereed) Published
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.
Place, publisher, year, edition, pages
2002. Vol. 531, no 2, 141-51 p.
Apoptosis, Bcl-2, Breast cancer, 2-Methoxyestradiol, Prostate cancer, Stress-activated protein kinase/c-Jun N-terminal kinase
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-65012DOI: 10.1016/S0014-5793(02)03478-6PubMedID: 12417302 OAI: oai:DiVA.org:uu-65012DiVA: diva2:92923