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. Author manuscript; available in PMC: 2011 Jan 24.
Published in final edited form as: Nature. 2007 Jan 7;445(7126):437–441. doi: 10.1038/nature05474

Figure 2. Forward shift in HER3 phosphorylation-dephosphorylation equilibrium following extended HER TKI treatment.

Figure 2

(A) BT474 cells were transfected with anti-HER2 (H) or control (C) siRNA and harvested 64 hours after transfection (lanes 1,2). Additional arms were treated with 48 hours of gefitinib untransfected (lanes 3,4) or following siRNA transfection (lanes 5,6). (B) SKBr3 cells were treated with 5μM gefitinib for 0,1, or 48 hours. Arm W was treated for 48 hours, washed, and incubated in drug-free media for one more hour. (C) SKBr3 cells were treated with the indicated concentrations of gefitinib for one hour (left side). Additional arms were treated with 5 μM gefitinib for 48 hours and subsequently treated with the indicated concentrations of gefitinib for one additional hour (right side). (D) SKBr3 cells were treated with the indicated concentrations and durations of PD168393. (E) SKBr3 cells were treated with 2 μM PD168393 for the indicated times. (F) SKBr3 cells were transfected with anti-HER3 (H) or control (C) siRNA and harvested 4 days after transfection (lanes 1,2). Additional arms were treated with gefitinib or control in untransfected cells (lanes 3,4) or following siRNA transfection (lanes 5,6). (G) In parallel with figure F, SkBr3 cells were either left untransfected, or transfected with anti-HER3 or control siRNA followed by 5uM gefitinib or control for 48 hours. Apoptotic cells were identified by their subG1 DNA content. (H) SKBr3 cells were treated as indicated for 48 hours. Apoptotic cells were identified by Annexin V expression.