IGF1R and gastric cancer: Moreover, in MKN45 gastric cancer cells transfected with MGAT5 (a cellular model known to induce changes in E-cadherin glycosylation and consequently in tumour cell behaviour[17]), we have demonstrated that the overexpression of GnT-V leads to an increased expression of the Insulin Receptor (Figure S3 E), which further supports the relationship between post-translational modifications of E-cadherin and IR/IGF-IR signaling in the process of tumour cell invasion.