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. 2015 Apr 1;106(5):550–558. doi: 10.1111/cas.12654

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© 2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Fig 1 — ERAP suppresses non-genomic signaling by the crosstalk between E2 and insulin-like growth factor 1 (IGF-1). (a) Luciferase assays showing the inhibitory effect of ERAP on the estrogen receptor alpha (ERα) transcriptional activity of MCF-7 cells by 10 nM E2 and 50 ng/mL IGF-1. These data represent the mean ± SD of three independent experiments (***P < 0.001). (b) The inhibitory effects of ERAP on the interactions of ERα with IGF-1Rβ and PI3K in the presence of E2 and IGF-1. (c–f) The inhibitory effects of ERAP on Akt (c, d), MAPK (c, d), and multiple ERα phosphorylations (e, f) induced by E2 and IGF-1 stimulation in MCF-7 (c, e) and BT-474 (d, f) cells. The data are expressed as the fold increase over untreated cells at 0 h. The above all blot were cropped, and the full-length blots are included in Supplementary Figure S4.