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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: J Hepatol. 2021 Jan 27;74(6):1429–1441. doi: 10.1016/j.jhep.2021.01.028

Figure 1. Increased STARD1 expressed in human NASH-driven HCC.

Figure 1.

A) Expression of STAR gene mRNA by qPCR and STARD1 protein in liver tissue from control donors and NASH-driven HCC (N of controls =15, N of HCC patients 15–20).

B) Representative immunohistochemical expression of STARD1 from control and NASH-HCC patient liver samples.

C) Staining of liver sections from control and HCC samples with GST-PFO (red) to detect free cholesterol. Nuclei were stained with DAPI.

D) Immunostaining of liver sections from control and HCC samples with GST-PFO and cytochrome c (Cyt C), showing their colocalization as merge and mask. Bar 75 μm.

E) Transcript quantification by qPCR of genes controlling cholesterol biosynthesis, ER stress-driven activation of SREBP2.

F) mRNA levels of HIF1A and HIF2A (EPAS1) and HIF-1α regulated genes. N of control 13–18, N of HC 13–20.

G) Hepatic levels of total BAs in samples from control and human HCC. (N=15 both groups).

All values are mean ± SEM. * indicate statistically significant differences between the indicated groups (p<0.05) in Student’s t test. Magnification bar in histology pictures, 100 μm.