Fig. 5

BMP4 regulates SLC2A1 expression through canonical SMAD signaling in Huh7 and HepG2 cells. A Huh7 and HepG2 cells were treated with 1 μM LDN193189 or equal volume DMSO, and PAS staining was subjected to evaluate glycogen accumulation after 72 h. B Huh7 and HepG2 cells were treated with 1 μM LDN193189 or equal volume DMSO, respectively. TqPCR analysis was carried out to detect the expression of GBE1, GYS1, PYGM, and UGP2 at 48 h. **P < 0.01, *P < 0.05, LDN193189 group vs DMSO group. C Huh7 and HepG2 cells were treated with Ad-B4, Ad-GFP, Ad-siB4, and Ad-RFP to overexpress or silence BMP4, respectively. TqPCR analysis was used to evaluate the expression of SMAD1/5/8 at 48 h. D The correlation of SMAD5 with SLC2A1 in LIHC data from TCGA tumor. E The correlation of SMAD5 with SLC2A1 in liver data from GTEx. F Huh7 and HepG2 cells were treated with Ad-B4, Ad-GFP, Ad-siB4, or Ad-RFP to overexpression or silence BMP4, respectively. Western blotting was used to analyze the expression of SMAD5 and p-SMAD5. G ChIP assay was conducted to verify that potential SMAD5 bind sites to the SLC2A1 promoter in Huh7 and HepG2 cells