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. Author manuscript; available in PMC: 2017 Jan 20.
Published in final edited form as: Oncogene. 2016 Jun 27;36(3):397–409. doi: 10.1038/onc.2016.211

Figure 5. Mitochondrial stress-induced HIF-1α activation in p53+/+ and p53−/− HCT116 cells.

Figure 5

(A) Immunoblot analysis of nuclear and cytosolic fractions with antibodies to HIF-1α and p53 in indicated cells. (B) The effects of ectopically expressed WT and R175H mutant p53 in H1299 prostate cancer cells which lack p53 expression. Details were as in Fig. 2D. Antibody to Laminin B1 used as a nuclear marker and antibody to GAPDH was used as cytoplasmic marker. The numbers in parentheses in A and B represent band intensities (average of two separate estimates). (C) ChIP analysis of EPO, VEGF and Glut-1 promoter regions for HIF-1α binding. Data represent Means ± S.E of three independent assay points. (D and E) mRNA levels for different glycolytic pathway genes in control and depleted p53+/+ and p53−/− cells (Fig. E) by realtime PCR. Means ± S.E. were calculated from 3 independent assays. ** indicates p<0.005 and *, p< 0.05. Values in parentheses of all immunoblots (average of two separate estimates) indicate relative band intensities normalized with relative GAPDH levels.