Publikation: Disruption of Tumor Cell Adhesion Promotes Angiogenic Switch and Progression to Micrometastasis in RAF-Driven Murine Lung Cancer
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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.
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CETECI, Fatih, Semra CETECI, Christiaan KARREMAN, Boris W. KRAMER, Esther ASAN, Rudolf GÖTZ, Ulf R. RAPP, 2007. Disruption of Tumor Cell Adhesion Promotes Angiogenic Switch and Progression to Micrometastasis in RAF-Driven Murine Lung Cancer. In: Cancer Cell. 2007, 12(2), pp. 145-159. ISSN 1535-6108. eISSN 1878-3686. Available under: doi: 10.1016/j.ccr.2007.06.014BibTex
@article{Ceteci2007-08Disru-38680, year={2007}, doi={10.1016/j.ccr.2007.06.014}, title={Disruption of Tumor Cell Adhesion Promotes Angiogenic Switch and Progression to Micrometastasis in RAF-Driven Murine Lung Cancer}, number={2}, volume={12}, issn={1535-6108}, journal={Cancer Cell}, pages={145--159}, author={Ceteci, Fatih and Ceteci, Semra and Karreman, Christiaan and Kramer, Boris W. and Asan, Esther and Götz, Rudolf and Rapp, Ulf R.} }
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