Fig. 2: Autocrine of the hedgehog signaling pathway.
From: Mechanisms and therapeutic potential of the hedgehog signaling pathway in cancer
A Ligand-Independent Activation: In this scenario, the HH pathway is activated without the presence of the HH ligand. The Patched (Ptch) receptor is inactive, allowing the Smoothened (Smo) protein to remain active. This leads to the activation of the Gli-A transcription factor, which then moves into the nucleus and promotes the transcription of target genes that drive cancer cell proliferation. B Ligand-Dependent Activation: Here, the HH pathway activation depends on the presence of the HH ligand. The HH ligand binds to the Ptch receptor, which results in the inhibition of Ptch activity. This inhibition allows Smo to activate, leading to the activation of the Gli-A transcription factor. Gli-A then translocates to the nucleus and induces the expression of target genes involved in cancer progression. Created with BioRender.com.
