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- W566379568 abstract "Abstract : An endocrine therapy is the most effective means to (initially) manage many hormone-dependent breast cancers. Unfortunately, almost 50% of estrogen receptor positive (ER+) breast cancers fail to respond (de novo resistant) and many others recur following an apparently initial response. We have now shown that cells respond to the stress of these therapies by activating the unfolded protein response (UPR). A central component of the UPR, and that which confers its prosurvival activities, is driven by the unconventional (cytosolic) splicing of XBP1 by the endoribonuclease function of IRE1. We screened small molecule libraries against IRE1 in silico and tested the top predicted hits for their abilities to inhibit XBP1s production and breast cancer cell proliferation, and to potentially reverse resistance to AEs. The most effective compound (N-(4-Phenoxy-phenyl)-2-(5-pyridin-3-yl-2H-[1,2,4]triazol-3-ylsulfanyl)-acetamide; NPPTA) was selected for further study and is the initial focus of this IDEA Expansion application." @default.
- W566379568 created "2016-06-24" @default.
- W566379568 creator A5005082206 @default.
- W566379568 date "2014-10-01" @default.
- W566379568 modified "2023-09-24" @default.
- W566379568 title "Targeting the UPR to Circumvent Endocrine Resistance in Breast Cancer" @default.
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- W566379568 doi "https://doi.org/10.21236/ada613724" @default.
- W566379568 hasPublicationYear "2014" @default.
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