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Review

Hedgehog signaling pathway in colorectal cancer: function, mechanism, and therapy

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Pages 3249-3259 | Published online: 30 Jun 2017

Figures & data

Figure 1 The sketch of Hedgehog (Hh) signaling pathway. The Hh signaling pathway contains three Hh homologs: Sonic Hh, Indian Hh, and Desert Hh. (A) When the ligand is absent (“Off” state), the patched (Ptc) receptor inhibits the downstream protein Smoothened (SMO). Henceforth, glioma-associated oncogene homolog (Gli) proteins are sequestered by Suppressor of Fused (SuFu). The Hh pathway is, generally, inhibited at “Off” state. (B) After activation of the Hh ligand, Hh proteins are released from the signaling cell. Hh then subsequently binds (“On” state) to PtcH, removing the inhibition and further activating SMO. SMO then regulates the downstream transduction molecules of Gli proteins (Gli1, Gli2, and Gli3). Gli proteins are subsequently transferred to the nuclei and they exert their transduction functions.

Figure 1 The sketch of Hedgehog (Hh) signaling pathway. The Hh signaling pathway contains three Hh homologs: Sonic Hh, Indian Hh, and Desert Hh. (A) When the ligand is absent (“Off” state), the patched (Ptc) receptor inhibits the downstream protein Smoothened (SMO). Henceforth, glioma-associated oncogene homolog (Gli) proteins are sequestered by Suppressor of Fused (SuFu). The Hh pathway is, generally, inhibited at “Off” state. (B) After activation of the Hh ligand, Hh proteins are released from the signaling cell. Hh then subsequently binds (“On” state) to PtcH, removing the inhibition and further activating SMO. SMO then regulates the downstream transduction molecules of Gli proteins (Gli1, Gli2, and Gli3). Gli proteins are subsequently transferred to the nuclei and they exert their transduction functions.

Table 1 Mutations that are correlated in colorectal carcinogenesis