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

Figure 6 EXT2 knockdown partly reverses the impact of SEL1L knockout in Huh7 cells. A: Western blot; B: Quantitative real-time polymerase chain reaction assay detected the efficiency of different siRNAs; C and D: Western blot analysis was conducted to assess the expression levels of EXT2, heavy-chain binding protein and inositol-requiring enzyme-1α following treatment; E: The proliferation of SEL1L knockout and EXT2 knockdown Huh7 cells was assessed using the cell counting kit-8; F and G: The proliferation of SEL1L knockout and EXT2 knockdown Huh7 cells was assessed using 5-Ethynyl-2’-deoxyuridine; H and I: The apoptosis rate of different Huh7 groups was detected by annexin V-fluorescein isothiocyanate/7-aminoactinomycin D staining; J: The proliferation of SEL1L knockout and EXT2 knockdown Huh7 cells was assessed using clone formation assays; K: The migration ability of SEL1L knockout and EXT2 knockdown Huh7 cells was detected by the transwell assay. ^aP < 0.05. ^bP < 0.01. ^cP < 0.001. ^dP < 0.0001. NS: Not significant; siNC: Small interfering RNA normal control; siRNA: Small interfering RNA; NC: Normal control; KO: Knockout; BiP: Heavy-chain binding protein; IRE-1α: Inositol-requiring enzyme-1α; 7AAD: 7-aminoactinomycin D staining; V-FITC: V-fluorescein isothiocyanate.