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Fig. 1 | Infectious Agents and Cancer

Fig. 1

From: Aflatoxin B1 inhibits the type 1 interferon response pathway via STAT1 suggesting another mechanism of hepatocellular carcinoma

Fig. 1

Establishing the maximum non-toxic concentration of AFB1 and maximum inducible concentration of rIFN-α (a) HepG2 cells were cultured at density of 5 × 104 cells per well of the 96-well plate until they reached 60% confluence. The cells were then treated with or without increasing amount of AFB1 (0–3200 μM) for 24 h after which the AFB1 containing media were replaced with fresh media. Cytotoxicity was evaluated by MTS-based assay at 24, 48 and 72 h. The viability of cells was calculated as ratio between AFB1 treated cells and non-treated cells. Data are presented as mean and standard deviation of three independent experiments each performed in duplicate wells, p-value ≤ 0.977 as determined by one-way ANOVA. b Establishing the maximal IFN-α induction of ISRE driven luciferase reporter gene activity. HepG2 cells were cultured at density of 5 × 104 cells per well of the 96-well plate until they reached 80% confluence. The cells were transiently co-transfected with pISRE-luc (500 ng) and pRLSV40 (1 ng). At 24 h post-transfection, the cells were treated with increasing concentration of rIFN-α. Luciferase activity was measured 24 h later. The data are presented as mean and the standard deviation of three independent experiments each conducted in duplicate wells. There was no significant difference in pISRE-luc activity of cells treated with 300 and 400 IU/ml of rIFN-α (p-value ≤ 0.7527)

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