| First Author | Engel NW | Year | 2016 |
| Journal | PLoS One | Volume | 11 |
| Issue | 11 | Pages | e0166690 |
| PubMed ID | 27902722 | Mgi Jnum | J:254192 |
| Mgi Id | MGI:6099567 | Doi | 10.1371/journal.pone.0166690 |
| Citation | Engel NW, et al. (2016) Canonical Wnt Signaling Drives Tumor-Like Lesions from Sox2-Positive Precursors of the Murine Olfactory Epithelium. PLoS One 11(11):e0166690 |
| abstractText | Canonical Wnt signaling is known to promote proliferation of olfactory stem cells. In order to investigate the effects of a constitutive activation of Wnt signaling in Sox2-positive precursor cells of the olfactory epithelium, we used transgenic mice that allowed an inducible deletion of exon 3 of the Ctnnb1 gene, which is responsible for the phosphorylation and degradation of Ctnnb1 protein. After induction of aberrant Wnt activation by Ctnnb1 deletion at embryonic day 14, such mice developed tumor-like lesions in upper parts of the nasal cavity. We still observed areas of epithelial hyperplasia within the olfactory epithelium following early postnatal Wnt activation, but the olfactory epithelial architecture remained unaffected in most parts when Wnt was activated at postnatal day 21 or later. In summary, our results suggest an age-dependent tumorigenic potential of aberrant Wnt signaling in the olfactory epithelium of mice. |
