Journal
CELL REPORTS
Volume 14, Issue 2, Pages 269-281Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.12.041
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Funding
- Department of Health via the National Institute for Health Research (NIHR) comprehensive Biomedical Research Centre
- King's College London
- Medical Research Council (MRC) [G1100073]
- Wellcome Trust [096540/Z/11/Z]
- European Union Framework 7 programme (HEALING)
- MRC
- EU-FP7 (HEALING)
- King's College Hospital NHS Foundation Trust
- MRC [MR/L022699/1, G1100073] Funding Source: UKRI
- Wellcome Trust [096540/Z/11/Z] Funding Source: Wellcome Trust
- Medical Research Council [MR/L022699/1, MC_PC_12009, G1100073] Funding Source: researchfish
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Wnt/beta-catenin activation in adult epidermis can induce new hair follicle formation and tumor development. We used lineage tracing to uncover the relative contribution of different stem cell populations. LGR6(+) and LRIG1(+) stem cells contributed to ectopic hair follicles formed in the sebaceous gland upon beta-catenin activation, whereas LGR5(+) cells did not. Lgr6, but not Lrig1 or Lgr5, was expressed in a subpopulation of interfollicular epidermal cells that were competent to form new hair follicles. Oncogenic beta-catenin expression in LGR5(+) cells led to formation of pilomatricomas, while LRIG1(+) cells formed trichoadenomas and LGR6(+) cells formed dermatofibromas. Tumor formation was always accompanied by a local increase in dermal fibroblast density and transient extracellular matrix remodeling. However, each tumor had a distinct stromal signature in terms of immune cell infiltrate and expression of CD26 and CD44. We conclude that compartmentalization of epidermal stem cells underlies different responses to beta-catenin and skin tumor heterogeneity.
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