Fig. 4

PPARα-SCD1 axis maintained CSC properties of spheres via promoting nuclear accumulation of β-Catenin. a Number of spheres derived from 1000 HCC cells which were treated with GW6471, PluriSln #1, or combination of clofibric acid (CA) and PluriSln #1 (left), and Relative expression of SCD1 in sphere cells after PPARα inhibition. b Number of spheres derived from 10000 primary HCC cells which were treated with GW6471, PluriSln #1, or combination of CA and PluriSln #. c Lefr panel: Representative photographs of parental HCC cells treated with DMSO for 5 days as controls, or parental HCC cells treated with 25 μM GW6471 for 5 days, or sphere HCC cells treated with 25 μM GW6471 for 2 days. Right panel: Representative photographs of parental HCC cells treated with DMSO for 5 days as controls, or parental HCC cells treated with 20 μM PluriSIn #1 for 5 days, or sphere HCC cells treated with 20 μM PluriSIn #1 for 2 days. d Fold changes of CSC-related markers of HCC sphere cells after treated with GW6471 (upper) or PluriSln #1 (lower) for 2 days. Results were normalized according to the expression of control spheres cells. e Representative immunofluorescence images of a Huh7 sphere co-stained with anti-β-Catenin and DAPI without (upper panel) or with (lower panel) SCD1 inhibition. f Fold changes of target genes of β-Catenin of Huh7 (upper) and Hep3B (lower) after treatment with PluriSln #1 for 2 days. Results were normalized according to the expression of control spheres cells. g Simplified diagram of present study. *: P < 0.05; ^**: P < 0.001