Biochemical pharmacologyNov 4, 2008

AHR signaling in prostate development, growth, and disease

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Apr 4, 2026

Abstract

Inappropriate activation of the aryl hydrocarbon receptor (AHR) due to early life exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) disrupts prostate morphogenesis.

AHR signaling is involved in prostate growth, morphogenesis, and disease.
TCDD pharmacologically activates AHR, affecting prostate development.
Crosstalk between AHR and steroid hormone receptors does not fully explain TCDD's effects on prostate morphogenesis.
AHR regulates the timing and patterning of prostate growth through interactions with developmental signals.
Early life TCDD exposure may lead to an increased risk of prostate disease in adulthood by impairing normal prostate development.
Recent studies indicate AHR's interactions with various signaling pathways, including WNT5A and fibroblast growth factor 10.

Simplified

Most evidence of aryl hydrocarbon receptor (AHR) signaling in prostate growth, morphogenesis, and disease stems from research using 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to pharmacologically activate the AHR at various stages of development. This review discusses effects of TCDD on prostate morphogenesis and highlights interactions between AHR and other signaling pathways during normal and aberrant prostate growth. Although AHR signaling modulates estrogen and androgen signaling in other tissues, crosstalk between these steroid hormone receptors and AHR signaling cannot account for actions of TCDD on prostate morphogenesis. Instead, the AHR appears to act within a cooperative framework of developmental signals to regulate timing and patterning of prostate growth. Inappropriate activation of AHR signaling as a result of early life TCDD exposure disrupts the balance of these signals, impairs prostate morphogenesis, and has an imprinting effect on the developing prostate that predisposes to prostate disease in adulthood. Mechanisms of AHR signaling in prostate growth and disease are only beginning to be unraveled and recent studies have revealed its interactions with WNT5A, retinoic acid, fibroblast growth factor 10, and vascular endothelial growth factor signaling pathways.

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AHR signaling in prostate development, growth, and disease

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