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. 2023 Feb 3;24(3):2962. doi: 10.3390/ijms24032962

Figure 5.

Figure 5

Persistently low GLI levels result in upregulation of GLI2 via FOXC1 in PTEN wild-type T-ALL cells. The schematic cartoon illustrates a possible mechanism of GLI2 upregulation via FOXC1/Akt/GSK-3β signaling. Upregulated FOXC1 activates Akt through a still undefined mechanism. Active Akt phosphorylates GSK-3β at Ser 9, thereby inhibiting GSK-3β which cannot target GLI2 for ubiquitination and proteasomal degradation. GLI2 translocates to the nucleus, where it upregulates a specific transcriptional program, resulting in extensive leukemic meningeal dissemination. FOXC1; Forkhead box C1; GSK-3β, glycogen synthase kinase 3β.