Breast Cancer Res Treat DOI 10.1007/s10549-016-3712-4
ERRATUM
Erratum to: Loss of glucocorticoid receptor activation is a hallmark of BRCA1-mutated breast tissue Myriam Vilasco1 • Laudine Communal1 • Justine Hugon-Rodin1,2 • Fre´de´rique Penault-Llorca3 • Najat Mourra4 • Zherui Wu1 • Patricia Forgez1 Anne Gompel1,2 • BRACAPS
•
Ó Springer Science+Business Media New York 2016
Erratum to: Breast Cancer Res Treat (2013) 142:283–296 DOI 10.1007/s10549-013-2722-8 In the original publication of the article, the blot corresponding to the total P38 protein content for the conditions siCtl and siBRCA1 in Fig. 7a was incorrectly laid out. The corrected Fig. 7a is given in this erratum.
The online version of the original article can be found under doi: 10.1007/s10549-013-2722-8. & Patricia Forgez
[email protected] & Anne Gompel
[email protected] 1
INSERM-UPMC Universite´ Paris 06, UMRS 938, Hoˆpital Saint Antoine, 75012 Paris, France
2
Unite´ de Gyne´cologie Endocrinienne, Universite´ Paris Descartes, AP-HP, Cochin Port Royal, 53, Avenue de l’Observatoire, 75014 Paris, France
3
Service d’Anatomie et Cytologie Pathologiques, Centre Jean Perrin, Clermont Ferrand, France
4
Service d’Anatomie et Cytologie Pathologiques, AP-HP, Hoˆpital Saint Antoine, 75012 Paris, France
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Ø
SB
siBRCA1
pcDNA3
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Ø
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BRCA1 wt
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siCtl
A
DEX+SB
Breast Cancer Res Treat
BRCA1 GR P-Ser211 GR P-p38 p38
BRCA1
GC
GR
GR
B P p38
p38 P Ser 211 GR GC
P Ser 211
GR
Nucleus Nucleus
GC
GRE GRE
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+
+
GR GR dependent dependent genes genes GR
Fig. 2 p38 pathway is involved in BRCA1-induced GR activity. a Representative immunoblot for BRCA1, GR P-Ser211, total GR, phospho-MAPK p38, and total MAPK p38 from MCF-7 cells silenced or overexpressing BRCA1. Cells were treated with 100 nM DEX in
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combination or not with 10 lg/ml SB 202190, a p38 inhibitor. b Potential mechanism as BRCA1 regulates GR expression and activity
