Fig. 3

Collagen I induced the activation of ERK in heat-exposed residual HCC cells. a The up-regulated level of ERK1/2 phosphorylation were induced in heat-exposed residual HCC cells cultured on collagen I versus Matrigel. The p-ERK content was normalized for ERK. b ERK1/2 inhibitor U0126 (25 μM) or sorafenib (5 μM) could reverse the collagen I-promoted proliferative, protrusive and spindle-like appearance of heat-treated residual HCC cells. c ERK1/2 inhibitor (U0126, 25 μM) or sorafenib (5 μM) reversed collagen I-mediated upregulation of ERK1/2 in heat-exposed residual HCC cells. Collagen I-induced upregulation of proliferation (PCNA), EMT (vimentin and N-cadherin), cancer stem cell marker Nanog was markedly reduced in heat-exposed residual HCC cells pretreated with ERK1/2 inhibitor (U0126, 25 μM) or sorafenib (5 μM). The p-ERK content was normalized for ERK. Expression levels of PCNA, vimentin, N-cadherin and Nanog were normalized to Tubulin