Fig. 5

TINCR relieves the repression of miR-195-3p on ST6GAL1, enhancing the NF kappa B Pathway. A, Relative mRNA (left) and protein (right) levels of ST6GAL1 in HepG2 and HuH7 cells transfected with miR-195-3p mimic or miR-Ctrl. B, Relative mRNA (left) and protein (right) levels of ST6GAL1 in HepG2 and HuH7 cells transfected with miR-195-3p inhibitor or anti-Ctrl. C, The predicted miR-195-3p binding sites in the ST6GAL1 transcript. The red nucleotides represent mutant sequences of target sites. D, The luciferase activities in HepG2 and HuH7 cells. E, Relative mRNA (left) and protein (right) levels of ST6GAL1 in HepG2 and HuH7 cells transfected with si-TINCRs or scrambled control. F, Relative mRNA (left) and protein (right) levels of ST6GAL1 in HepG2 and HuH7 cells transfected with pcDNA3.1-TINCR or empty vector. G, Correlation between TINCR and ST6GAL1 expression based on the GEO database (GSE54236). H-I, Western blot analysis of expression of ST6GAL1 and phosphorylation levels of IκBα (p-IκBα) and p65 (p-p65) in HepG2 cells cotransfected with si-TINCR #2 or scrambled control together with miR-195-3p inhibitor or anti-Ctrl (H), and pcDNA3.1-TINCR or empty vector together with miR-195-3p mimic or miR-Ctrl (I). Data are expressed as the mean ± SD of at least three independently repeated experiments. *P < 0.05; **P < 0.01; ***P < 0.001