Type VII collagen is required for ras-driven human epidermal tumorigenesis

Susana Ortiz-Urda, John Garcia, Cheryl L. Green, Lei Chen, Qun Lin, Dallas P. Veitch, Lynn Y. Sakai, Hyangkyu Lee, M. Peter Marinkovich, Paul A. Khavari

Research output: Contribution to journalArticlepeer-review

120 Scopus citations


Type VII collagen defects cause recessive dystrophic epidermolysis bullosa (RDEB), a blistering skin disorder often accompanied by epidermal cancers. To study the role of collagen VII in these cancers, we examined Ras-driven tumorigenesis in RDEB keratinocytes. Cells devoid of collagen VII did not form tumors in mice, whereas those retaining a specific collagen VII fragment (the amino-terminal noncollagenous domain NC1) were tumorigenic. Forced NC1 expression restored tumorigenicity to collagen VII-null epidermis in a nori-cell-autonomous fashion. Fibronectin-like sequences within NC1 (FNC1) promoted tumor cell invasion in a laminin 5-dependent manner and were required for tumorigenesis. Tumor-stroma interactions mediated by collagen VII thus promote neoplasia, and retention of NC1 sequences in a subset of RDEB patients may contribute to their increased susceptibility to squamous cell carcinoma.

Original languageEnglish (US)
Pages (from-to)1773-1776
Number of pages4
Issue number5716
StatePublished - Mar 18 2005

ASJC Scopus subject areas

  • General


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