Hedgehog Signaling in Development and Cancer 2021

Dear Colleagues,

The canonical Hh signaling pathway involves binding a secreted molecule (Hedgehog, Hh) to a 12-span-protein receptor (Patched, Ptch). In the absence of the Hh ligands, the Ptch receptor inhibits a seven-span-transmembrane receptor (Smoothened, 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).

The primary cilium plays a central role in the transduction of Hh signals in vertebrates. Hh pathway components continuously traffic through the cilium. In Hh’s absence, the Ptch receptor localizes to the primary cilium, inhibiting Smo activation and preventing Smo accumulation to the cilia. When Hh binds to Ptch, Ptch activity is blocked, leading to the accumulation of Smo in the cilium and activation of downstream signaling pathways.

The Hedgehog pathway represents a key regulator of embryonic development, tissue homeostasis, tissue repair, and stem cell maintenance. Dysregulation of the Hh signaling pathway is associated with developmental anomalies and various cancer types. Mutations leading to cell-autonomous activation of the Hedgehog pathway in primary tumor cells drive tumor growth in a ligand-independent way in familial cancers such as basal cell carcinoma (BCC), medulloblastoma (MB), and rhabdomyosarcoma (RM). In contrast, several recent studies have shown a surprisingly general effect of stromal Hh response in restraining cancer growth and progression, most notably in the bladder, pancreatic, colon, prostate, and lung cancers. 

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. Xiaoyan Zheng
Guest Editor

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