p23 Modulates Aryl Hydrocarbon Receptor Protein Levels in Normal Cell Lines

Aryl hydrocarbon receptor (AHR) is a transcription factor activated in response to exposure of environmental toxins. p23, a co‐chaperone of AHR, was found to be capable of regulating ligand‐dependent AHR activation and functions. Previous study from our laboratory showed that low expression of the p23 protein is associated with poor AHR protein stability and function in cancer cell lines. While in a p23 null mouse model, it was reported that p23 did not affect the AHR expression. To better understand this apparent dichotomy, we explored the possibility that the AHR expression may be regulated differently in cancer cells than in normal cells. We analyzed the AHR protein levels in three normal cell lines with either wild‐type or reduced p23 protein levels (55–62% of the wild‐type p23 protein levels), namely human breast epithelial cells (MCF‐10A), human bronchial tracheal epithelial cells (HBTEC), and mouse type I regulatory T cells (Tr1). We observed that the AHR expression was significantly reduced by about 38–57% compared to the controls after 72 hours transfection of p23‐specific shRNA in all three normal cells, indicating that p23 is more important for the control of AHR expression in normal conditions than previously expected. In conclusion, our data clearly support that p23 is necessary in maintaining the AHR protein levels in normal and cancer cells. Insights on underlying mechanisms and implications will be presented and discussed. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .