Abstract

Splicing of X-box binding protein1 (XBP1) is implicated in up-regulation of estrogen receptors leading to antiestrogen resistance in breast cancer. Unfolded protein response (UPR) is an adaptive survival mechanism in cancer cells, where XBP-1 splicing is induced. UPR can either increase the folding capacity of cells or initiate apoptosis when the misfolded protein burden is overwhelming. We hypothesized that therapeutic LOFU would induce protein misfolding, increase endoplasmic reticulum stress and sensitize breast tumor cells to tamoxifen.

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