AHR regulates miR-29b. (A) Illustration depicting 2 predicted AHR-binding consensus sequences, also known as DREs, in the miR-29b promoter, highlighted in the red boxes. pGL3 luciferase reporter plasmids were cloned into HepG2 cells with seed sequence for either CYP1A1 (positive control) or miR-29b (B), miR-29a/b1 or miR-29b2/c (C), or miR-29b with the 5′ AHR site or the 3′ AHR binding site within the miR-29b promoter mutated (D). Each group was then treated with DMSO or FICZ (an AHR agonist). (E) pGL3 luciferase reporter plasmids were cloned into the miR-29b promoter in HepG2 cells, and AHR was knocked down in the same cells. The scrambled control (siCTRL) and the siAHR were treated with DMSO or FICZ and luciferase was measured. (F) CD56⁺/Lineage negative NK cells were isolated from PB and treated with vehicle DMSO vehicle control or FICZ. ChIP was performed with anti-AHR or isotype control antibody. The anti-AHR ChIP product was evaluated for miR-29b promoter expression in by qPCR to validate association between AHR and the miR-29b promoter. Data reported as expression relative to control. (G) Primary PB allogeneic NK cells were cultured with either media only or AML conditioned media, and miR-29b ChIP was performed similar to panel F. Minimum of 2 independent studies performed with representative figures depicted. *P < .05; ***P < .0001. Error bars indicate SD.