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Fig. 6 | BMC Cancer

Fig. 6

From: β-arrestin1-mediated acetylation of Gli1 regulates Hedgehog/Gli signaling and modulates self-renewal of SHH medulloblastoma cancer stem cells

Fig. 6

Schematic overview of Arrb1 and miR-326 role in CSCs. Left: Arrb1 and miR-326 expression are downregulated in CSCs derived from SHH-MB. These molecular features have a role in the maintenance of Hh/Gli signaling in CSCs. Right: Arrb1/miR-326 levels increase following exposure to differentiation signals (DFM) or after ectopic re-expression. Arrb1 protein enhances p300-induced acetylation of Gli1 (Gli-Ac) reducing its transcriptional activity. miR-326 targets and represses Smo and Gli2 mRNAs resulting in a blunted Hh/Gli signaling. The consequent low Hh/Gli signaling induces stemness impairment, growth arrest and facilitates differentiation of CSCs

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