Fig. 6: Transcriptionally activation of beclin-1 by FOXO3a is essential for hypoxia-induced autophagy in HCC cells. | Cell Death & Disease

Fig. 6: Transcriptionally activation of beclin-1 by FOXO3a is essential for hypoxia-induced autophagy in HCC cells.

From: Hypoxia induces sorafenib resistance mediated by autophagy via activating FOXO3a in hepatocellular carcinoma

Fig. 6

A Detection of binding status of FOXO3a to beclin-1 promotor by ChIP in HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) cultured in normoxia or in hypoxia (Normoxia vs. Hypoxia, ***p < 0.001; t-test). B Schematic representation of wild-type (WT) beclin-1 promoter and its mutations (MUT). Detection of the relative mRNA level of luciferase in beclin-1 WT LM-3 cells (LM-3 cells transfected with luciferase reporter plasmid containing FOXO3a binding element of beclin-1 promotor) or beclin-1 MUT LM-3 cells (LM-3 cells transfected with luciferase reporter plasmid containing mutant FOXO3a binding element of beclin-1 promotor) cultured in normoxia or in hypoxia by RT-PCR (Normoxia vs. Hypoxia, ***p < 0.001; t-test). C Western blot analysis of p62 and LC-3 in HCC cells (Huh-7, LM-3, SNU-387, and SNU-449) transfected with si-beclin-1 cultured in hypoxia. D Western blot analysis of p62 and LC-3 in LM-3 cells transfected with transfected with FOXO3a-ΔDBD (transcription-inactive FOXO3a plasmid) cultured in hypoxia. E Western blot analysis of p62 and LC-3 in HCC cells (Huh-7 and SNU-449) transfected with si-FOXO1 cultured in hypoxia. Each experiment was performed in triplicate (N = 3). The data are presented as the means ± SD.

Back to article page