Abstract
Furthermore, LR cell lines proliferated by E1S in dose-dependent manner more than their parental cells, but there was no difference of proliferation when estrone and estradiol treated. STS inhibitor administered with letrozole was inhibitory to proliferation of LR cells. LR cells were also inhibited by SERM and SERD. In mRNA analysis of clinical primary tissues of postmenopausal patients, expression of STS mRNA significantly correlated with those of three OATPs which were induced in LR cell lines. Conclusion: In this study, we first demonstrated that the contribution of E1S to ER-positive breast cancer in the context of AI resistance. Targeting therapy to E1S–STS pathway could present a new choice of treatments to AI-resistant breast cancer patients, especially by combination with AI. Disclosure of Interest: No significant relationships.
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