article title: akt-aro and her2-aro, models for de novo resistance to aromatase inhibitors;...
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Article Title: AKT-aro and HER2-aro, models for de novo resistance to aromatase inhibitors; molecular characterization and inhibitor response studies Journal Name: Breast Cancer Research and Treatment Author Names and Affiliations: Cynthie Wong1, Xin Wang1, David Smith2, Kaladhar Reddy3 and Shiuan Chen1
1Division of Tumor Cell Biology, 2Department of Information Sciences, Beckman Research Institute of the City of Hope, Duarte, CA 91010, 3Department of Pathology, Wayne State University, Detroit, MI 48201
Corresponding author email address: [email protected]
Supplementary Table 1; Wong, Wang, Smith, Reddy and Chen
Kinetic analysis of aromatase activity
Cell line Vmax (nmol/mg/h) Km (nM)
MCF-7aro 16.97 ± 0.89 18.85 ± 1.28
AKT-aro 5.4 ± 0.11 9.18 ± 2.24
HER2-aro 9.72 ± 0.60 20.67 ± 6.39
Aromatase kinetic analysis was carried out in triplicate. Mean ± SD are shown.
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Supplementary Figure 1; Wong, Wang, Smith, Reddy and Chen
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Supplementary Figure 1. 17-DMAG induces G2 phase arrest. Cells were treated with either DMSO or 100 nM 17-DMAG for 24, 48, or 72 h. a) AKT-aro and b) HER2-aro cells were stained with propidium iodide and analyzed by flow cytometry.
AKT-aro HER2-aro
Supplementary Figure 2; Wong, Wang, Smith, Reddy and Chen
Supplementary Figure 2. 17-DMAG suppresses ER activity. The pGL3-(ERE)3 reporter plasmid was transiently transfected into MCF-7aro, AKT-aro and HER2-aro cell lines. Cell lines were treated with either DMSO or 100 nM 17-DMAG, in addition to 1 nM E2 for 48 hours. Data (mean ± SD) is representative of 3 independent experiments performed in triplicate.