Figure 6.

Impact of oral sodium tungstate treatment on cell cycle progression and DNA damage response in the AOM/DSS model. Groups of C57BL/6 mice were treated i.p. with 20 mg/kg AOM. After 7 d, animals received streptomycin (2 mg/ml in the drinking water) and were intragastrically inoculated with the colibactin-producing E. coli NC101 2 d later. Mice were treated for 1 wk with 2% DSS (n = 14), 2% DSS supplemented with 0.2% sodium tungstate (DSS+W, n = 13), or filtered drinking water (mock, n = 5). Animals were allowed to recover for 4 d. Colonocytes were isolated, total RNA was extracted, and relative mRNA levels of marker genes were determined by quantitative RT-PCR. Data from two independent experiments are shown. (A) Schematic representation of the experiment. (B) mRNA levels of Ercc1 and Mlh1, whose gene products are involved in DNA damage response. (C) mRNA levels of Trp53, encoding the tumor suppressor p53. (D) mRNA levels of Cdk4, Cdk6, and Ccnd1, whose products are involved in cell cycle progression. Bars represent the geometric mean ± 95% confidence interval. P values were calculated by unpaired, two-tailed Student’s t test on log-transformed data. *, P < 0.05; **, P < 0.01; ***, P < 0.001.