| First Author | Perl AK | Year | 1998 |
| Journal | Nature | Volume | 392 |
| Issue | 6672 | Pages | 190-3 |
| PubMed ID | 9515965 | Mgi Jnum | J:46388 |
| Mgi Id | MGI:1197805 | Doi | 10.1038/32433 |
| Citation | Perl AK, et al. (1998) A causal role for E-cadherin in the transition from adenoma to carcinoma. Nature 392(6672):190-3 |
| abstractText | Development of malignant tumours is in part characterized by the ability of a tumour cell to overcome cell-cell adhesion and to invade surrounding tissue. E-cadherin is the main adhesion molecule of epithelia, and it has been implicated in carcinogenesis because it is frequently lost in human epithelial cancers. Re-establishing the functional cadherin complex in tumour cell lines results in a reversion from an invasive to a benign epithelial phenotype. However, it remained unresolved whether the loss of E-cadherin-mediated cell adhesion was a cause or a consequence of tumour progression in vivo. Here we report that the loss of E-cadherin expression coincides with the transition from well differentiated adenoma to invasive carcinoma in a transgenic mouse model of pancreatic beta-cell carcinogenesis (Rip1Tag2). Intercrossing Rip1Tag2 mice with transgenic mice that maintain E- cadherin expression in beta-tumour cells results in arrest of tumour development at the adenoma stage, whereas expression of a dominant- negative form of E-cadherin induces early invasion and metastasis. The results demonstrate that loss of E-cadherin-mediated cell adhesion is one rate-limiting step in the progression from adenoma to carcinoma. |
