| Literature DB >> 29925428 |
Kheng Tian Lim1, Niamh Cosgrave1, Arnold David Hill1,2, Leonie S Young3.
Abstract
After the publication of this work [1] errors were noticed in the total protein loading controls for Figs. 1C, 2B, 3B and 4B.Entities:
Year: 2018 PMID: 29925428 PMCID: PMC6011587 DOI: 10.1186/s13058-018-0987-x
Source DB: PubMed Journal: Breast Cancer Res ISSN: 1465-5411 Impact factor: 6.466
Fig. 1Effect 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)
Fig. 217β-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)
Fig. 3Effect 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)
Fig. 4The 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)