Hedgehog Signaling in Development and Cancer

Dear Colleagues,

The canonical Hh signaling pathway involves the binding of a secreted molecule (Hedgehog, Hh) to a 12-span- protein receptor (Patched, Ptch). In the absence of an Hh ligand, the Ptch receptor inhibits a seven-span-transmembrane receptor (Smoothned, Smo), while upon ligand binding, Ptch releases Smo from its inhibition, triggering a cascade of signaling, culminating in the activation of a family of zinc finger transcription factors glioma-associated oncogene (Gli).

In vertebrates, the Hh pathway is localized at the primary cilium, where it undergoes a dynamic trafficking with Ptch located at the cilium membrane in the absence of Hh ligand and Ptch internalization upon Hh binding, with consequent Smo translocation to the cilium membrane and transduction of downstream Hh signaling.

The Hedgehog pathway represents a key regulator of embryonic development and tissue homeostasis as well as of tissue repair and maintenance of stem cells. Recent studies have demonstrated that Hh signaling is activated in a ligand-independent way in familial cancers such as basal cell carcinoma, medulloblastoma, and rhabdomyosarcoma, as a consequence of genetic aberrations deleting the Ptch inhibitory receptor or activating Smo receptor as well as a consequence of Gli amplification, while in sporadic cancers, Hh pathway activation occurs in a ligand- independent noncanonical way, as a result of a crosstalk with other oncogenic pathways or as a consequence of a ligand-dependent autocrine or paracrine way.

This Special Issue offers an Open Access forum that aims to bring together a collection of original research articles, reviews, and communications on the function of Hh signaling in development, human cancers, and diseases, as well as on the role of Hh signaling molecules as diagnostic, prognostic, and therapeutic targets.

Dr. Maria Domenica Castellone
Guest Editor

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