Suppression of colon cancer stemness by CDX1/2 through inhibition of β-catenin-facilitated Pol II complex formation (IMAGE)

University of Fukui

Suppression of colon cancer stemness by CDX1/2 through inhibition of β-catenin-facilitated Pol II complex formation

Caption

This scheme illustrates a hypothetical model of the transcriptional mechanism controlling colon cancer stemness by stable β-catenin and CDX1/2, via DSIF and PAF1C complexes. Stable β-catenin promotes colon cancer stemness by enhancing the recruitment of DSIF and PAF1C complexes to the Pol II complex. Conversely, these processes are suppressed by CDX1 and CDX2, which are intestine-specific transcription factors

Credit

Prof. Koji Aoki from the University of Fukui, Japan

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