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Increasing epidemiological and animal experimental data provide substantial support for the role of aryl hydrocarbon receptor (AhR) in mammary tumorigenesis. The effects of AhR have been clearly demonstrated in rodent models of breast carcinogenesis and in several established human breast cancer cell lines following exposure to AhR ligands or AhR overexpression. However, relatively little is known about the role of AhR in human breast cancers. AhR has always been considered to be a regulator of toxic and carcinogenic responses to environmental contaminants such as TCDD (dioxin) and benzo[a]pyrene (BaP). The aim of this study was to identify the type of breast tumors (ERα-positive or ERα-negative) that express  AHR  and how AhR affects human tumorigenesis. The levels of  AHR ,  AHR  nuclear translocator ( ARNT ) and  AHR  repressor ( AHRR ) mRNA expression were analyzed in a cohort of 439 breast tumors, demonstrating a weak association between high  AHR  expression and age greater than fifty years and ERα-negative status, and HR-/ERBB2 breast cancer subtypes.  AHRR  mRNA expression was associated with metastasis-free survival, while  AHR  mRNA expression was not. Immunohistochemistry revealed the presence of AhR protein in both tumor cells (nucleus and/or cytoplasm) and the tumor microenvironment (including endothelial cells and lymphocytes). High  AHR  expression was correlated with high expression of several genes involved in signaling pathways related to inflammation ( IL1B ,  IL6 ,  TNF ,  IL8  and  CXCR4 ), metabolism ( IDO1  and  TDO2  from the kynurenine pathway), invasion ( MMP1 ,  MMP2  and  PLAU ), and IGF signaling ( IGF2R ,  IGF1R  and  TGFB1 ). Two well-known ligands for  AHR  (TCDD and BaP) induced mRNA expression of  IL1B  and  IL6  in an ERα-negative breast tumor cell line. The breast cancer ER status likely influences AhR activity involved in these signaling pathways. The mechanisms involved in AhR activation and target gene expression in breast cancers are also discussed.

plos one

High AHR expression in breast tumors correlates with expression of genes from several signaling pathways namely inflammation and endogenous tryptophan metabolism