Fig. 3: Elevated VDAC2 and Bak expression in human liver cancer.

A Relative VDAC2 and Bak1 protein levels in 31 normal human tissues by quantitative mass spectrometry⁴⁷, normalized by the estimated mitochondrial content of each tissue. Values for brain samples from cerebellum and cortex and heart samples from atrium and ventricle are indicated. B Relative VDAC1 and VDAC2 protein levels in human tissues, normalized by the estimated mitochondrial content as in (A). C Immunoblots (left) of VDAC2 and Bak in paired HCC and normal tissue samples resected from patients (see Supplementary Table 1); prohibitin as mitochondrial loading control. Quantification of changes in VDAC2:prohibitin and Bak:prohibitin, normalized by the average log₂ ratio of the normal samples. Statistical significance from two-sided paired t-test is indicated. SDS-PAGE and immunoblot was performed twice with similar results. D vdac2 and bak gene expression fold increases and percentage ranks in normal versus cancer comparisons across five mRNA databases available from Oncomine as of 2018. At right, heatmap for rank of each gene; hsp9a (mitochondrial HSP70) was used as a mitochondrial gene control. Gray indicates that the transcript was not measured in the Chen study. p values from Wilcoxon Rank Sum test. E Differences in vdac2 and bak mRNA in 214 HCC patients from the Roessler Liver 2 dataset⁴⁸, calculated by subtracting the log₂ values (normalized using the Robust Multi-Array Average method and global median centering) in tumor from the value in the liver sample taken from the same patient. Percentages represent the fraction of patients in that quadrant. F Differences in VDAC2 and Bak protein levels (after normalization for mitochondrial content) in 159 paired tumor and liver samples from⁴⁹. Source data are provided in the Source Data file.