Abstract

Although Aryl hydrocarbon receptor (AhR) may be critical to several types of cancers, the function of AhR for carcinogenesis of bladder cancer (BC) is still inconclusive. We, therefore, sought to examine the involvement of AhR in bladder carcinogenesis. We examined the AhR expression of human BC and N-butyl-N-(4-hydroxybutyl)-induced bladder carcinogenesis in AhR-deficient mice. There was a significantly higher expression of AhR in non-muscle-invasive BC compared to normal tissue and muscle-invasive BC (MIBC). The incidence of MIBC in AhR-deficient mice (87.5%) was significantly higher than wild-type mice (9.5%, p<0.01). In cell invasion assay, the induction of AhR signaling resulted in attenuation of BC cell invasiveness and proliferation. These results suggest that AhR may be essential for the initiation of carcinogenesis and attenuated the invasion of BC cells; this signaling may have a dual function in bladder carcinogenesis.

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