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Article

Partial truncation of the C-terminal domain of PTCH1 in cancer promotes tumourigenesis by non-canonical activation of a GLI-PI3K loop.

Oncogene - 1 Mar 2026

Caballero-Ruiz Begoña, Bordone Rosa, Coni Sonia, Gkotsi Danai S, Gonzalez Eva, Canettieri Gianluca, Riobo-Del Galdo Natalia A

Abstract excerpt

Loss of function mutations of the Hedgehog receptor PTCH1 are oncogenic drivers in some skin and brain cancers. We recently reported mutations in exons encoding the C-terminal tail of PTCH1 in colon cancer, which result in premature truncation but do not impair canonical Hedgehog signalling. In this study, we show that colon cancer cells engineered by CRISPR/Cas9 to express endogenous truncated PTCH1 have...

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Topics

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Share to Carcinogenesis
Share to Cell Proliferation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Colonic Neoplasms

Share to Gene Expression Regulation, Neoplastic

Share to Hedgehog Proteins

Share to Patched-1 Receptor

Share to Phosphatidylinositol 3-Kinases

Share to Zinc Finger Protein GLI1

Source

Open in PubMed Open full text

Identifiers

PMID: 41748949
DOI: 10.1038/s41388-026-03698-9
PMCID: PMC12987731

Genes

PTCH1
EGFR
GLI1
GLI2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

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Partial truncation of the C-terminal domain of PTCH1 in cancer promotes tumourigenesis by non-canonical activation of a GLI-PI3K loop.PMID 41748949Read ↗

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