The exogenous E-cadherin expression in MDA-MB-435 cells (which endogenously lack E-cadherin expression at both the mRNA and protein levels) inhibits IR, IGF-IR and downstream ERK 1/2 phosphorylation, whereas stimulation of MDA-MB-435+E-cad cells with insulin and IGF-I decreases the bisected N-glycan expression (in general and specifically on E-cadherin), up-regulates mesenchymal markers and enhances tumor cell invasion [42]. Here, CDH1 is linked to neoplasm.