Fig. 3: c-MYC directly regulates PDK2 expression.
From: The OGT–c-Myc–PDK2 axis rewires the TCA cycle and promotes colorectal tumor growth
Quantitative PCR analysis (A) and immunoblotting analysis (B) of PDK2 expression in HT-29 and HCT116 cells infected with scramble or shc-Myc. n = 3; Data are presented as means ± SD. P values were determined by unpaired two-tailed Student’s t tests. C Dual-luciferase reporter assay showing the effects of c-Myc overexpression on relative PDK2-promoter activity in the 293 T cells. n = 3; Data are presented as means ± SD. P values were determined by unpaired two-tailed Student’s t tests. D ChIP-qPCR analysis of c-Myc binding to the predicted binding regions of PDK2 promoter in HT-29 cells. Ectopic c-Myc was pulled down by the anti-c-Myc antibody. n = 3; Data are presented as means ± SD. P values were determined by unpaired two-tailed Student’s t tests. E Cell proliferation of HT-29 and HCT116 infected with Scramble, shc-Myc or shc-Myc reconstituted with PDK2 expression. n = 5; Data are presented as means ± SD. P values were determined by unpaired two-tailed Student’s t tests. F Xenograft analysis of HT-29 cells expressing Scramble, shc-Myc, shPDK2 or shc-Myc reconstituted with PDK2 expression. Images of dissected tumors from mice. Analysis of tumor growth (G), tumor weights (H) and Ki67 staining (I) of tumors generated from HT-29 cells infected with scramble, shc-Myc, shPDK2 or shc-Myc reconstituted with PDK2 expression. Scale bars: 100 μm. Quantification was shown. n = 5; Data are presented as means ± SD. P values were determined by unpaired two-tailed Student’s t tests.
