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Oestrogen-mediated suppression of tumour necrosis factor alpha-induced apoptosis in MCF-7 cells: Subversion of Bcl-2 by anti-oestrogens



Oestrogen-mediated suppression of tumour necrosis factor alpha-induced apoptosis in MCF-7 cells: Subversion of Bcl-2 by anti-oestrogens



Journal of Steroid Biochemistry and Molecular Biology 78(5): 409-418



In oestrogen receptor (ER)-positive breast carcinoma cells, 17beta-oestradiol suppresses a dose-dependent induction of cell death by tumour necrosis factor alpha (TNF). The ability of oestrogens to promote cell survival in ER-positive breast carcinoma cells is linked to a coordinate increase in Bcl-2 expression, an effect that is blocked with the pure anti-oestrogen ICI 182,780. The role of Bcl-2 in MCF-7 cell survival was confirmed by stable overexpression of Bcl-2 which resulted in suppression of apoptosis induced by doxorubicin (DOX), paclitaxel (TAX) and TNF as compared to vector-control cells. The pure anti-oestrogen ICI 182,780 in combination with TNF, DOX or TAX potentiated apoptosis in vector-transfected cells. Interestingly, pre-treatment with ICI 182,780 markedly enhanced chemotherapeutic drug- or TNF-induced apoptosis in Bcl-2 expressing cells, an effect that was correlated with ICI 182,780 induced activation of c-Jun N-terminal kinase. Our results suggest that the effects of oestrogens/anti-oestrogens on the regulation of apoptosis may involve coordinate activation of signalling events and Bcl-2 expression.

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Accession: 011084026

Download citation: RISBibTeXText

PMID: 11738551

DOI: 10.1016/s0960-0760(01)00117-0


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