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. 2019 Sep 9;18(5):4377–4384. doi: 10.3892/ol.2019.10826

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Copyright: © Jeng et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 1. — Shh signaling pathway in hepatocellular carcinoma. Left (Off state): Ptch inhibits SMO activation. The signaling from SMO to Gli is blocked. SuFu binds to Gli for protein degradation via the proteasome. Therefore, the expression of Hh signaling pathway target gene turns off. Right (On state): Shh ligand bind to their receptor, PTCH. The binding of Hh ligands to PTCH weakens the inhibition of SMO and activates signal transduction via GLI transcription factor, activating downstream gene expression in cell migration/invasion/transition (SNAIL, MMPs, CHSY1), cell cycle/tumor growth (cyclin B1, CDK, Bcl2) and cancer stem cell marker (CD133). Shh, Sonic hedgehog; Ptch, protein patched homolog; SMO, smoothened homolog; Gli, glioma associated oncogene homolog; EMT, epithelial-mesenchymal transition.