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Fig. 2 | Infectious Agents and Cancer

Fig. 2

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

Fig. 2

AFB1 inhibits IFN-α induced ISRE signalling in a dose dependent fashion. 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). The pRL40-luc which constitutively expresses the Renilla luciferase was included as internal control to which pISRE-luc activity was normalized. At 24 h post-transfection, the cells were stimulated with or without rIFN-α and simultaneously treated with or without AFB1. Transfected cells which were stimulated with rIFN-α but not treated with AFB1 were calculated to have 100% pISRE-luc activity. The data are presented as mean normalized pISRE-luc activity and the standard deviation of three independent experiments each conducted in duplicate wells. There was a significant difference in pISRE-luc activity of cells stimulated with rIFN-α alone compared to cells stimulated with rIFN-α and simultaneously treated with 10 μM of AFB1 (p-value ≤ 0.047)

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