Fig. 4

BMP4-induced glycogen synthesis can be blocked by SLC2A1 inhibitor in Huh7 and HepG2 cells. A Different doses of BAY-876 were used to treat Huh7 and HepG2 cells, and cell proliferation was assessed at 0, 24, 48, and 72 h by WST-1. B 1 μm BAY-876 or equal volume DMSO was used to treated Huh7 and HepG2 cells, and TqPCR analysis was carried out to detect the expression of key enzymes of glycogenesis GBE1, GYS1, UGP2, and glycogenolysis PYGM at 48 h. **P < 0.01, **P < 0.05, 0 (DMSO) group vs 1 μm group. C Ad-B4 was used to infect Huh7 and HepG2 cells and treated with 1 μm BAY-876 or equal volume DMSO, and PAS staining was subjected to evaluate glycogen accumulation after 72 h. D Ad-B4 was used to infect Huh7 and HepG2 cells and treated with 1 μm BAY-876 or equal volume DMSO. The glycogen content assay was subjected to evaluate glycogen level after 72 h. **P < 0.01, Ad-B4 + DMSO group vs Ad-B4 + BAY-876 group. E Huh7 and HepG2 cells were infected with Ad-B4 and treated with 1 μm Bay-876 or equal volume DMSO, respectively. TqPCR analysis was carried out to detect the expression of GBE1, GYS1, PYGM, and UGP2 at 24 h and 48 h, respectively. **P < 0.01, *P < 0.05, Ad-B4 + DMSO group vs Ad-B4 + BAY-876 group. F The correlation of BMP4 with GBE1, GYS1, PYGM, and UGP2 in LIHC data from TCGA tumor