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. 2017 Nov 20;8(62):106038–106049. doi: 10.18632/oncotarget.22524

Figure 8. rFAM3C inactivated FOXO1 and repressed gluconeogenic gene expression in HSF1-dependent manner.

Figure 8

Cells were treated with 5ng/ml rFAM3C for 24 hours in the absence or presence of KRIBB11. (A) rFAM3C promoted the nuclear exclusion of FOXO1 in HSF1-dependent manner in HepG2 cells. The images were the representatives of 3 experiments. (B) rFAM3C repressed PEPCK protein expression in HSF1-dependent manner in HepG2 cells. (C) rFAM3C repressed gluconeogenesis in HSF1-dependent manner in HepG2 cells. Con, control cells; rFAM3C, cells treated with rFAM3C. N=4-5, *P<0.05 versus control cells, #P<0.05 versus rFAM3C-treated cells without inhibitor.