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The transcriptional factor, DACH1, functions as tumor suppressor by antagonizing FOX protein signaling

The Dachshund gene (dac) was originally cloned in Drosophila as a dominant inhibitor of ellipse and encodes a key component of the RDGN. Altered expression or function of mammalian RDGN components have been described in human tumors. DACH1 is thought to regulate gene expression by complexing with DNA‐binding transcription factors. Crystal structure reveals that DACH1 containing a DNA binding motif similar to that found in the winged helix/forkhead subgroup of DNA binding proteins, however, no sequence‐specific DNA binding of DACH1 has been identified so far. Herein, CAST identified a DACH1 DNA‐binding sequence which resembles the FOX (Forkhead Box containing protein) binding site. Genome‐wide in‐silico promoter analysis of DACH1 binding sites identified gene clusters populating cellular pathways associated with the cell cycle and growth factor signaling. ChIP‐Seq mapped DACH1 binding sites to corresponding gene clusters predicted in silico and identified as weight matrix resembling the CAST‐defined sequence. DACH1 antagonized FOXM1 target gene expression, promoter occupancy in the context of local chromatin, and contact‐independent growth. Proteomic analysis identified CA150 as the transcriptional co‐regulator of DACH1 activity. Attenuation of FOX function by the cell fate determination pathway has broad implications given the diverse role of FOX proteins in cellular biology and tumorigenesis.