Figure 4

Over-expression of AP-2γ significantly upregulated the transcription activities of ErbB2, CDH2, HPSE and IGSF11. Luciferase vectors of wild-type or mutant AP-2γ-ChIP-fragments were cotransfected with pCMV-Myc-AP-2γ or pCMV-Myc into MDA-MB-453, MDA-MB-231, and HBL-100 cells, and luciferase gene expression was assayed. A. Wild-type R3-1/ErbB2 was upregulated by AP-2γ in different breast cancer cells. B. Mutation on AP-2γ binding site of CDH2 abrogated the upregulation by AP-2γ. C. Disruption of binding site on R3-36/HPSE (648–656) reduced the upregulation of HPSE by AP-2γ; "however the binding site on R3-36/HPSE (676–684) is not functional. D. Mutation of binding site R1-15-286/IGSF11 inhibited the upregulation of IGSF11 by AP-2γ in different breast cancer cells. The relative luciferase activity in each sample was normalized and presented as mean ± SD from triplicated independent experiments. (* means P < 0.01).