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. Author manuscript; available in PMC: 2022 May 28.
Published in final edited form as: Cancer Lett. 2021 Mar 6;506:95–106. doi: 10.1016/j.canlet.2021.03.002

Figure 2. IRF-1 promotes CXCL10 transcription.

Figure 2.

CXCL10 mRNA expression is defined by qRT-PCR in Hepa1–6 cells (A) and Huh-7 cells (B) infected by mouse / human AdIRF-2 (50 MOI) for 48 h with or without mouse IFN-γ (50 u/ml) / human IFN-γ (100 u/ml) for 12 h, respectively. C) Schematic representation of IRF-1 binding sites in the human CXCL10 promoter region as predicted by PROMO bioinformatics software. D) ChIP assay is performed with IgG or anti IRF-1 antibody in cell lysis from Huh-7 cells which are induced by human IFN-γ (250 u/ml) for 6 h. The qPCR analyses of immunoprecipitated DNA are conducted using the primers which are designed to amplify the indicated region of the CXCL10 promoter. Each data point (A & B) represents an independent experiment (n=3). Data (A, B & D) represent the mean ± SD, *p<0.05, **p<0.01. ChIP-qPCR assay results shown are statistical difference from four independent experiments. E) Luciferase activity from IFN-γ (250 u/ml) induced HepG2 cells transfected with wild type (WT) CXCL10 promoter construct (but not mutated ISRE CXCL10 promoter construct) is significantly increased (**p<0.01, NS not significant). F) IRF-2 significantly reduces luciferase activity from IFN-γ stimulated wild type CXCL10 promoter construct (*p<0.05 by ANOVA). Luciferase assays shown are representative of four experiments with similar results.