SEL1L-mediated endoplasmic reticulum associated degradation inhibition suppresses proliferation and migration in Huh7 hepatocellular carcinoma cells

Figure 1 Endoplasmic reticulum-associated protein degradation inhibitor treatment significantly inhibited the growth of Huh7 cells. A: Time course and concentration course of endoplasmic reticulum-associated protein degradation (ERAD) inhibitor treatment; B: Heavy-chain binding protein mRNA expression at different time points and concentrations of the inhibitor; C: Protein expression at different time points and concentrations of the inhibitor; D: The proliferation of Huh7 cells in the dimethyl sulfoxide (DMSO) and ERAD inhibitor groups was assessed using cell counting kit-8; E: The proliferation of Huh7 cells in the dimethyl sulfoxide and ERAD inhibitor groups was assessed using 5-Ethynyl-2’-deoxyuridine; F: The apoptosis rate of Huh7 cells treated with DMSO or the ERAD inhibitor was assessed using annexin V-fluorescein isothiocyanate/7-aminoactinomycin D staining; G: The proliferation of Huh7 cells in the DMSO and ERAD inhibitor groups was assessed using clone formation assays; H: The migration ability of DMSO or ERAD inhibitor treated Huh7 cells was detected by the transwell assay. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. ^dP < 0.0001. DMSO: Dimethyl sulfoxide; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; BiP: Heavy-chain binding protein; EerI: Eeyarestatin I; 7AAD: 7-aminoactinomycin D staining; V-FITC: V-fluorescein isothiocyanate.