Fig. 3From: Coordinated activation of DNMT3a and TET2 in cancer stem cell-like cells initiates and sustains drug resistance in hepatocellular carcinomaRole of DNMT3a and TET2 in resistant cell growth. SorafenibR Hep3b and Huh7 cells were infected with DNMT3a or TET2 shRNA or control viruses and selected by 2 µg/ml puromycin for 5 days. a and b, qPCR (a) and Western blotting (b) assessing efficacy of DNMT3a knockdown. Data represents three independent experiments, and the graphs are shown as mean values ± S.D. c and d, Dotblotting measuring changes of DNA methylation or hydroxymethylcytosine using 5mC and 5hmC antibodies. The graphs (d) are the quantification of dot intensity shown as mean values ± S.D. from three independent experiments. e and f, Proliferation (e) and migration (f) assays in resistant cells 5 days after virus infection in drug-free medium. Data represents two independent experiments with 12 repeats in total. g and h, qPCR (g) and Western blotting (h) showing TET2 knockdown. Data represents three independent experiments. i and j, Dotblotting measuring changes in DNA methylation or hydroxymethylcytosine using 5mC and 5hmC antibodies (i). The graphs (j) are the quantification of dot intensity as mean values ± S.D. from three independent experiments. k and l, Proliferation (k) and migration (l) assays in resistant cells 5 days after virus infection in drug-free medium. Data represents two independent experiments with 12 repeats in total. *P < 0.05; ns, not significantBack to article page