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Contents lists available at ScienceDirect
Journal of Steroid Biochemistry and Molecular Biology
journal homepage: www.elsevier.com/locate/jsbmb
A novel SRC-2-dependent regulation of epithelial-mesenchymal transition in T breast cancer LY3009120
Olivera Bozickovica,b,d,1, Linn Skartveitb,1, Agnete S.T. Engelsenc, Thomas Hellandb, Kristin Jonsdottirf, Marianne Hauglid Flågengb, Ingvild S. Fenneb, Emiel Jansseng, James B. Lorensc, Lise Bjørkhaugb,d,e, Jørn V. Sagena,b,d, Gunnar Mellgrena,b,d,
a Department of Clinical Science, University of Bergen, N-5021 Bergen, Norway
b Hormone Laboratory, Haukeland University Hospital, N-5021 Bergen, Norway
c Centre for Cancer Biomarkers (CCBIO), Department of Biomedicine, University of Bergen, N-5009 Bergen, Norway
d KG Jebsen Center for Diabetes Research, Department of Clinical Science, University of Bergen, N-5021 Bergen, Norway r> e Department of Biomedical Laboratory Sciences, Western Norway University of Applied Sciences, N-5020 Bergen, Norway
f Department of Pathology, Stavanger University Hospital, N-4068 Stavanger, Norway
g Department of Mathematics and Natural Sciences, University of Stavanger, N-4036 Stavanger, Norway
Steroid receptor coactivator 2 (SRC-2) is a nuclear receptor coactivator, important for the regulation of estrogen receptor alpha (ERα)-mediated transcriptional activity in breast cancer cells. However, the transcriptional role of SRC-2 in breast cancer is still ambiguous. Here we aimed to unravel a more precise transcriptional role of SRC-2 and uncover unique target genes in MCF-7 breast cancer cells, as opposed to the known oncogene SRC-3. Gene expression analyses of cells depleted of either SRC-2 or SRC-3 showed that they transcriptionally regulate mostly separate gene sets. However, individual unique gene sets were implicated in some of the same major gene ontology biological processes, such as cellular structure and development. This finding was supported by three-dimensional cell cultures, demonstrating that depletion of SRC-2 and SRC-3 changed the morphology of the cells into epithelial-like hollow acinar structures, indicating that both SRC proteins are involved in maintaining the hybrid E/M phenotype. In clinical ER-positive, HER2-negative breast cancer samples the expression of SRC-2 was negatively correlated with the expression of MCF-7-related luminal, cell cycle and cellular morphogenesis genes. Finally, elucidating SRC-2 unique transcriptional eﬀects, we identified Lyn kinase (an EMT biomarker) to be upregulated exclusively after SRC-2 depletion. In conclusion, we show that both SRC-2 and SRC-3 are es-sential for the EMT in breast cancer cells, controlling diﬀerent transcriptional niches.