This was paralleled by enhanced expression of phosphorylated Erk1/2. POSTN induced the activation of ERK1/2 in heat-treated HCC residual cells and increased the expression of PCNA and N-cadherin whereas ERK inhibitor abolished POSTN-induced ERK phosphorylation and the upregulation of PCNA and N-Cadherin (Fig. 3d). As previously described, POSTN promotes tumor development through integrin receptors [30]. Here, CDH2 is linked to neoplasm.