Molecular aspects of antiestrogen resistance and autophagy in breast cancer cells

TL;DRAbstract

The major objective of this thesis was to examine the molecular aspects of estrogenic growth and autophagy in estrogen receptor α (ERα)-positive breast cancer cells. We first examined the role of autophagy mediator, Beclin 1, in estrogenic signaling and antiestrogen resistance in Beclin 1-overexpressing MCF-7 cells. We found that a potential interaction between ERα and Beclin 1 rendered Beclin 1-transfected cells less sensitive to estradiol (E2)-induced growth stimulation, and to antiestrogen-mediated growth inhibition. Thus, a novel function for Beclin 1 might involve down-regulation of the action of ERα, contributing to resistance of breast cancer cells to antiestrogens.In an attempt to develop novel therapeutic agents for breast cancer, we explored the effect of the polyamine analogue, 1,15-bis(ethylamino)-4,8,12-triazapentadecane (BE-3-3-3-3), on MCF-7 cell growth in the presence and absence of E2. BE-3-3-3-3 caused growth inhibition in the presence of E2. However, it mimicked estr

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