Figure 7
From: Foxm1 controls a pro-stemness microRNA network in neural stem cells
Regulation of cerebellar NSC self-renewal by the Hh-Foxm1-miRNA axis. Increased Hh-Gli signalling promotes NSC self-renewal by inhibiting p53 and upregulating Nanog expression. The tumour-suppressor p53 checks NSC self-renewal directly, by activating Trp53inp1, and by inhibiting Gli and Nanog. Our data show (bold-face type) that Hh-Gli signalling also upregulates the expression of Foxm1 (directly and indirectly via Nanog). The targets of these two transcription factors include a number of miRNAs that regulate the expression of important genes, including Trp53inp1. Repression of Trp53inp1 disrupts a feedback loop that maintains high p53 levels, thereby diminishing the tumour suppressor’s ability to repress Gli and Nanog expression.
