Fig. 6: LncRNA NEAT1/EZH2/LATS2 activates the Hippo/YAP signaling pathway.

The protein expression patterns of YAP1 in HL-7702 cells treated with D-GalN/LPS quantified by western blot analysis (a). Quantification of protein expression in a (b). The binding relationship between YAP1 and P73, assessed by coIP (c). *p < 0.05 vs. the D-GalN/LPS+oe-NC group; #p < 0.05 vs. the D-GalN/LPS+sh-NC group. D-GalN/LPS+oe-NC group, HL-7702 cells treated with oe-NC in the presence of D-GalN/LPS treatment; D-GalN/LPS+sh-NC group, HL-7702 cells treated with sh-NC in the presence of D-GalN/LPS treatment; D-GalN/LPS+oe-NEAT1 group, HL-7702 cells treated with oe-NEAT1 in the presence of D-GalN/LPS treatment; D-GalN/LPS+oe-LATS2 group, HL-7702 cells treated with oe-LATS2 in the presence of D-GalN/LPS treatment; D-GalN/LPS+sh-NEAT1 group, HL-7702 cells treated with sh-NEAT1 in the presence of D-GalN/LPS treatment; D-GalN/LPS+sh-LATS2 group, HL-7702 cells treated with sh-LATS2 in the presence of D-GalN/LPS treatment. Statistical data are described as mean ± standard deviation. One-way analysis of variance was used for comparisons among multiple groups, followed by Tukey’s post hoc test. The experiment was repeated three times independently. lncRNA NEAT1 long noncoding RNA nuclear-enriched abundant transcript 1, LATS2 large tumor-suppressor kinase 2, D-GalN/LPS, D-galactosamine/lipopolysaccharide, NC negative control, coIP coimmunoprecipitation.