Cited by 612Wnt/β-catenin signaling in development and cancerCancer and Skin LesionsHedgehog Signaling Pathway Studies

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A common human skin tumour is caused by activating mutations in β-catenin

Chan, Edward, Gat, Uri, McNiff, Jennifer M, Fuchs, Elaine·1999·Nature Genetics

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Abstract

WNT signalling orchestrates a number of developmental programs. In response to this stimulus, cytoplasmic beta-catenin (encoded by CTNNB1) is stabilized, enabling downstream transcriptional activation by members of the LEF/TCF family. One of the target genes for beta-catenin/TCF encodes c-MYC, explaining why constitutive activation of the WNT pathway can lead to cancer, particularly in the colon. Most colon cancers arise from mutations in the gene encoding adenomatous polyposis coli (APC), a protein required for ubiquitin-mediated degradation of beta-catenin, but a small percentage of colon and some other cancers harbour beta-catenin-stabilizing mutations. Recently, we discovered that transgenic mice expressing an activated beta-catenin are predisposed to developing skin tumours resembling pilomatricomas. Given that the skin of these adult mice also exhibits signs of de novo hair-follicle morphogenesis, we wondered whether human pilomatricomas might originate from hair matrix cells and whether they might possess beta-catenin-stabilizing mutations. Here, we explore the cell origin and aetiology of this common human skin tumour. We found nuclear LEF-1 in the dividing tumour cells, providing biochemical evidence that pilomatricomas are derived from hair matrix cells. At least 75% of these tumours possess mutations affecting the amino-terminal segment, normally involved in phosphorylation-dependent, ubiquitin-mediated degradation of the protein. This percentage of CTNNB1 mutations is greater than in all other human tumours examined thus far, and directly implicates beta-catenin/LEF misregulation as the major cause of hair matrix cell tumorigenesis in humans.

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Authors: Chan, E., Gat, U., McNiff, J. M., & Fuchs, E.
Affiliations: Howard Hughes Medical Institute (US)
Yale University (US)
Corresponding author: Fuchs, Elaine
ORCID: McNiff, Jennifer M
Fuchs, Elaine
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 1999-04
Volume: 21
Issue: 4
Pages: 410-413
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/7747
OpenAlex: W1484268538
Cited by: 612
References: 31
Citations by year: 2026: 8 · 2025: 5 · 2024: 7 · 2023: 13 · 2022: 12 · 2021: 9 · 2020: 19 · 2019: 12 · 2018: 10 · 2017: 20 · 2016: 18 · 2015: 14 · 2014: 26 · 2013: 24 · 2012: 27
FWCI: 15.75
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Genetics (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIH-RO1-AR31737, R01AR031737)
National Institute of Dental and Craniofacial Research (NCI-P50DE/CA-11921)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Health Sciences › Medicine › Dermatology › Cancer and Skin Lesions
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Hedgehog Signaling Pathway Studies
Keywords: pilomatrixoma, β-catenin, CTNNB1 mutation, Wnt signaling, LEF1, hair matrix cells, skin tumours, tumor cell of origin, hair follicle morphogenesis, transgenic mice, c-Myc, APC, carcinogenesis
MeSH terms: Amino Acid Sequence, Cytoskeletal Proteins, DNA-Binding Proteins, Gene Frequency, Hair Diseases, Humans, Molecular Sequence Data, Mutation, Skin Neoplasms, Transcription Factors, Deoxyribonucleases, Type II Site-Specific, Trans-Activators, Polymerase Chain Reaction, Sequence Analysis, DNA, Pilomatrixoma, beta Catenin, Lymphoid Enhancer-Binding Factor 1

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A common human skin tumour is caused by activating mutations in β-catenin

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