List of abbreviations: DDA: dendrogenin A; 5,6-EC:
5,6-epoxycholesterol; 5,6α-EC: 5,6α-epoxycholesterol; 5,6β-EC:
5,6β-epoxycholesterol; CT: Cholestane-3β,5α,6β-triol; OCDO:
6-oxo-cholestan-3β,5α-diol ; AEBS: microsomal antioestrogen binding
site; D8D7I: 3β-hydroxyterol-Δ8-Δ7-isomerase; EPB: emopamyl binding
protein; DHCR7: 3β-hydroxyterol-Δ7-reductase; ChEH:
cholesterol-5,6-epoxide hydrolase; HSD11B1: 11β-hydroxysteroid
dehydrogenase type 1; H6PD, HSD11B2: 11β-hydroxysteroid dehydrogenase
type 2; ER: estrogen receptor; LXR: liver-X-receptor; GR: glucocorticoid
receptor; BC: breact cancer; ER(+)BC: oestrogen receptor positive BC;
TNBC, triple negative BC; HER2: Epithelial Growth Factor Receptor of
type 2; SERM: selective ER modulators; AI: aromatase inhibitors; 27-HC:
27-hydroxycholesterol; CXCR2: C-X-C Motif Chemokine Receptor 2;
SULT2B1b: hydroxysteroid sulfotransferase 2B1b; CYP27A1: Cytochrome P450
Family 27 Subfamily A Member 1; 5,6-ECS:
5,6α-epoxy-cholesterol-3β-sulfate; zymostenol: cholest-8-ene-3β-ol.
Aknowledgement: We thank members of the ENOR consortium
for fruitful discussions.
Competing interests: The authors declare no competing
financial
interests.
Funding: This work was funded by an internal grant from the
‘Institut National de la Santé et de la Recherche Médicale’ and the
‘Université de Toulouse III’, the Fondation de France (R11166BB), the
Association pour la Recherche sur le Cancer (PJA 2013 12 00 342), the
INCA translational (PRTK-K15-118), the INCA (PLBIO-2018-145), the
Fondation Toulouse Cancer Santé (2017CS065); and the associations
“Céline”, “Flo” and ”Elles” for their generous support.