| First Author | Ceteci F | Year | 2007 |
| Journal | Cancer Cell | Volume | 12 |
| Issue | 2 | Pages | 145-59 |
| PubMed ID | 17692806 | Mgi Jnum | J:124321 |
| Mgi Id | MGI:3721330 | Doi | 10.1016/j.ccr.2007.06.014 |
| Citation | Ceteci F, et al. (2007) Disruption of Tumor Cell Adhesion Promotes Angiogenic Switch and Progression to Micrometastasis in RAF-Driven Murine Lung Cancer. Cancer Cell 12(2):145-159 |
| abstractText | Progression of non-small-cell lung cancer (NSCLC) to metastasis is poorly understood. Two genetic approaches were used to evaluate the role of adherens junctions in a C-RAF driven mouse model for NSCLC: conditional ablation of the cdh1 gene and expression of dominant-negative (dn) E-cadherin. Disruption of E-cadherin caused massive formation of intratumoral vessels that was reversible in the early phase of induction. Vascularized tumors grew more rapidly, developed invasive fronts, and gave rise to micrometastasis. beta-catenin was identified as a critical effector of E-cadherin disruption leading to upregulation of VEGF-A and VEGF-C. In vivo, lung tumor cells with disrupted E-cadherin expressed beta-catenin target genes normally found in other endodermal lineages suggesting that reprogramming may be involved in metastatic progression. |
