The role of the cell adhesion molecule E-cadherin in cetuximab sensitivity of gastric cancer cell lines

The transition from benign to invasive and metastatic tumors is characterized by loss of cell-cell adhesion. In gastric cancer, the cell adhesion molecule E-cadherin is frequently mutated and consequently functionally inactivated.

E-cadherin interacts with EGFR in a multicomponent complex and negatively influences the receptor activation, whereas somatic mutation of E-cadherin is associated with increased activation of EGFR (Bremm et al., Cancer Res., 2008). The crosstalk between EGFR and E-cadherin is potentially relevant for tumor progression and response to EGFR-targeted therapy, for instance with the EGFR antibody cetuximab.

In this project we investigate the role of E-cadherin in cetuximab sensitivity of gastric cancer cell lines.

The project was initially funded in 2012-2013 by the ANTON & PETRA EHRMANN-Stiftung.