FIGURE 1.

c-Myc does not regulate expression of genes induced by PI 3-kinase inhibition. A, proliferating T98G cells were treated for 30, 60, and 120 min with LY294002. Protein extracts were immunoblotted with c-Myc and β-actin antibodies. B, ChIPs were performed with anti-Max, anti-Myc, or control rabbit IgG, using actively proliferating T98G cells that were treated with DMSO (vehicle control) or LY294002 for 30 min (for Myc binding). MYOG is a negative control. Data are presented as % input genomic DNA and are the mean ± S.E. of 3 samples. Binding of Max was significantly higher than the IgG control at all E-box sites (p < 0.05 by t test using S.D.). Positions of the E-box sites are shown in Fig. 5. C, actively proliferating T98G cells were transfected with c-Myc siRNA. Data are presented as the fold-difference in expression between cells transfected with c-Myc siRNA compared with nonspecific control siRNA and are the mean ± S.E. of 3 independent transfections. Knockdown of c-Myc protein was 70% (see inset).