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. 2023 Dec 22;9:467. doi: 10.1038/s41420-023-01755-w

Fig. 8. iCDM-34 induces AhR signaling based on AhR knockdown and CDK1 overexpression experiments.

Fig. 8

A, B HCV replicon cells were transfected with control and AhR siRNA. After 2 days of transfection, the cells were treated with 30 μM iCDM-17, iCDM-34, and CDM-3008 for 2 days. HCV replicon RNA levels were measured using a luciferase assay (A). Cell viability was measured using an XTT assay (B). C, D HCV replicon cells were transfected with control and CDK1 expression vectors. After 2 days of transfection, the cells were treated with 30 μM iCDM-17, iCDM-34, and CDM-3008 for 2 days. HCV replicon RNA levels were measured using a luciferase assay (C). Cell viability was measured using an XTT assay (D). Error bars indicate the SD (n = 3). The data are presented as the means ± SD. *p < 0.05 and **p < 0.01 based on two-tailed Student’s t test. n.s. indicates not significant. E iCDM-34 induces AhR activation and anti-HBV and anti-HCV activities via SAMHD1. iCDM-34 activates AhR which suppresses CDK1/2 expression, and SAMHD1 promotes the transition of dNTP to dN. Decreased dNTP levels inhibit HCV replicon RNA, HBV DNA, and pgRNA synthesis.