Supplementary Figure 5: Response of MEFs with different p53 genotypes to statins.
From: DNAJA1 controls the fate of misfolded mutant p53 through the mevalonate pathway
(a) WB for p53 and vinculin using E1A/H-RasG12V-transformed p53+/+, p53+/R172H, and p53R172H/R172H MEFs treated with DMSO, lovastatin (L, 4 μM), or atorvastatin (A, 4 μM) for 24 h. (b) Quantitative RT-PCR for p21 and PUMA using mRNA from E1A/H-RasG12V-transformed MEFs treated with (+) or without (−) 0.5 μM of doxorubicin for 24 h. Data are shown as relative mRNA expression to that of GAPDH. Error bars, means ± s.d. (n = 3 independent experiments), ∗∗P < 0.01, ∗P < 0.05, NS: not significant; Student’s t test (two-tailed). (c) Colony formation assays using transformed MEFs (500) treated with D or L (4 μM) for 10 days. Representative images (left) and a summarized graph (right). Error bars, means ± s.d. (n = 3 independent experiments), ∗∗P < 0.01; Student’s t test (two-tailed). (d) Representative images of IHC for p53, Ki67, and cleaved caspase 3 using transformed MEFs-derived tumors treated with D or A (magnification, ×40). Scale bar, 50 μm. Statistics source data for b and c are provided in Supplementary Table 1.
