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  • Open Access

Correction to: Nongenomic oestrogen signalling in oestrogen receptor negative breast cancer cells: a role for the angiotensin II receptor AT1

  • Kheng Tian Lim1,
  • Niamh Cosgrave1,
  • Arnold David Hill1, 2 and
  • Leonie S. Young1Email author
Breast Cancer Research201820:61

https://doi.org/10.1186/s13058-018-0987-x

Received: 14 May 2018

Accepted: 14 May 2018

Published: 20 June 2018

The original article was published in Breast Cancer Research 2006 8:R33

Correction

After the publication of this work [1] errors were noticed in the total protein loading controls for Figs. 1C, 2B, 3B and 4B. These errors do not affect the interpretation of the data. The corrected figures are shown below. We apologize for this error.
Figure 1
Fig. 1

Effect of 17β-oestradiol and EGF on cell proliferation and induction of MAPK protein expression in breast cancer cells. (c) SKBR3 breast cancer cells were treated with 5, 10 and 50 ng/ml EGF and 17β-oestradiol (10− 8 mol/l) alone and in combination for 10 min. 40 μg protein was electrophoresed on a 10% gel and transferred to nitrocellulose. The membrane was probed with rabbit anti-Phospho-Erk1/2 antibody (Thr202/Tyr204 - Cell Signalling # 4370) and mouse anti-Erk1/2 antibody (Cell Signalling # 4696)

Figure 2
Fig. 2

17β-oestradiol and EGF induced cell proliferation and raf phosporylation is mediated through EGFR. (b) SKBR3 and MCF-7 breast cancer cells were pre-treated with the EGFR antagonist AG1478 (150 nmol/l) for 1 h before 10 min of incubation with EGF (10 ng/ml) and 17β-oestradiol (10− 8 mol/l) alone and in combination. 40 μg protein was electrophoresed on a 10% gel and transferred to nitrocellulose. The membrane was probed with rabbit anti-Phospho-Raf antibody (Ser259 - Cell Signalling # 9421) and mouse anti-Raf antibody (Santa Cruz sc-373,722)

Figure 3
Fig. 3

Effect of GPCR antagonism on 17β-oestradiol and EGF induced cell proliferation, raf phosporylation and cAMP production in breast cancer cells. (b) SKBR3 and MCF-7 cells were pre-treated with the GPCR antagonist pertussis toxin (50 ng/ml) for 1 h before 10 min of incubation with EGF (10 ng/ml) and 17β-oestradiol (10− 8 mol/l) alone and in combination. 40 μg protein was electrophoresed on a 10% gel and transferred to nitrocellulose. The membrane was probed with rabbit anti-Phospho-Raf antibody (Ser259 - Cell Signalling # 9421) and mouse anti-Raf antibody (Santa Cruz sc-373,722)

Figure 4
Fig. 4

The role of the AT1 receptor in 17β-oestradiol and EGF mediated cell proliferation and raf phosphorylation breast cancer cells. (b) SKBR3 cells were pre-treated with the AT1 antagonist saralasin (10− 6 mol/l) for 1 h before 10 min of incubation with EGF (10 ng/ml) and 17β-oestradiol (10− 8 mol/l) alone and in combination. 40 μg protein was electrophoresed on a 10% gel and transferred to nitrocellulose. The membrane was probed with rabbit anti-Phospho-Raf antibody (Ser259 - Cell Signalling # 9421) and mouse anti-Raf antibody (Santa Cruz sc-373,722)

Notes

Declarations

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

Authors’ Affiliations

(1)
School of Medicine and Medical Science, St. Vincent’s University Hospital, Dublin, Ireland
(2)
School of Medicine and Medical Science, UCD Conway Institute of Biomolecular and Biomedical Research, UCD Conway Institute, University College Dublin, Dublin, Ireland

Reference

  1. Lim KT, Cosgrave N, Hill AD, Young LS. Nongenomic oestrogen signalling in oestrogen receptor negative breast cancer cells: a role for the angiotensin II receptor AT1. Breast Cancer Res. 2006;8(3):R33.View ArticlePubMedPubMed CentralGoogle Scholar

Copyright

© The Author(s). 2018

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