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Ammonium is a metabolic waste product mainly detoxified by the liver. Hepatic dysfunction can lead to cytotoxic accumulation of circulating ammonium and to subsequent encephalopathy. Transmembrane ammonium transport is a widely spread process ensured by the highly conserved proteins of the Mep-Amt-Rh superfamily, including the mammalian Rhesus (Rh) factors. The regulatory mechanisms involved in the control of  RH  genes expression remain poorly studied. Here we addressed the expression regulation of one of these factors,  RHBG . We identify HepG2 hepatocellular carcinoma cells and SW480 colon adenocarcinoma cells as expressing  RHBG  and show that its expression relies on β-catenin signaling. siRNA-mediated β-catenin knockdown resulted in significant reduction of  RHBG  mRNA in both cell lines. Pharmaceutical inhibition of the TCF4/β-catenin interaction or knockdown of the transcription factor TCF4 also downregulated  RHBG  expression. We identify a minimal  RHBG  regulatory sequence displaying a promoter activity and show that β-catenin and TCF4 bind to this fragment  in vivo . We finally characterize the role of potential TCF4 binding sites in  RHBG  regulation. Taken together, our results indicate  RHBG  expression as a direct target of β-catenin regulation, a pathway frequently deregulated in many cancers and associated with tumorigenesis.

Wnt/β-Catenin Signaling Regulates the Expression of the Ammonium Permease Gene RHBG in Human Cancer Cells