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. 2021 Feb 18;23:26. doi: 10.1186/s13058-021-01402-1

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — In vitro generated fulvestrant-resistant breast cancer cells downregulate ER signaling and proliferate independently of estrogen. a Dose-response curves for parental (-P, black lines) and fulvestrant-resistant (-FR, red lines) cells from six different breast cancer cell lines in response to 6-day treatment with fulvestrant (1 pM to 100 μM). Graphs represent combined data (average ± SEM) from two biological experiments with three technical replicates each. IC50 values are reported in Additional file 3C. b ERE reporter activity in parental and fulvestrant-resistant CAMA-1, MCF7, and HCC1428 cells after treatment for 24 h with (+F) or without (-F) supplementation of 100 nM fulvestrant. Graphs represent combined data (average ± SEM) from two biological experiments with two technical replicates each. Statistical differences were determined with one-way ANOVA and Tukey’s post-hoc test, *** represents p value ≤ 0.0001 between untreated parental and fulvestrant-resistant cells. Data for the ZR-75-1, T47D, and EFM-19 models are shown in Additional file 3E. c Western blotting for ERα expression in parental and fulvestrant-resistant CAMA-1, MCF7, and HCC1428 cells after treatment for 24 h with 100 nM fulvestrant (+F) or DMSO (-F). Representative data from three biological replicates. β-actin or β-tubulin was used as loading control. Quantification of band intensities is presented in Additional file 4A. Data for the ZR-75-1, T47D, and EFM-19 models are shown in Additional file 3F. d Proliferation curves for parental and fulvestrant-resistant CAMA-1, MCF7, and HCC1428 cells in estrogen-depleted media with (+F) or without (ctrl) supplementation of 100 nM fulvestrant. Graphs represent combined data (average ± SEM) from two biological experiments with three technical replicates each. Statistical differences were determined with two-way ANOVA and Tukey’s post-hoc test, *** represents p value ≤ 0.0001 and * ≤0.05 between untreated parental (black solid lines) and fulvestrant-resistant (red solid lines) cells at given time-points