Fig. 6

ST6GAL1 is responsible for TINCR-mediated cell progression and oxaliplatin insensitivity. A-B, CCK-8 assay of HepG2 (A) and HuH7 (B) cells cotransfected with si-TINCR 2# or scrambled control together with pc-DNA3.1-ST6GAL1 or empty vector. C-D, Representative images (C), and quantification (D) of the colony formation assay in the above-mentioned transfected cells. E, Quantification of transwell migration and invasion assays in the above-mentioned transfected cells. F, Representative images (left, only showed HepG2) and quantification (right) of the apoptosis assay of oxaliplatin (16 μg/ml) in transfected HepG2 and HuH7 cells. G-H, Western blot analysis of expression of ST6GAL1 and NF-kappa-B-related markers in HepG2 cells cotransfected with si-TINCR #2 or scrambled control together with pcDNA3.1-ST6GAL1 or empty vector (G), and pcDNA3.1-TINCR or empty vector together with si-ST6GAL1 or scrambled control (H). I, Mechanism model of the TINCR/miR-195-3p/ST6GAL1 axis and its effect on NF-kappa B Signaling. Data are expressed as the mean ± SD of at least three independently repeated experiments. *P < 0.05; **P < 0.01; ***P < 0.001