Figure 7.

Working model of the role of IL-6/STAT3 pathway on hypoxia promoting HCC progression after TACE. Hypoxia secondary to TACE hyperactivated IL-6/STAT3 signaling on residue HCC cells. More p-STAT3 was trans-located into nucleus of HCC cells and bound with the promoter of IL-6 and HIF-1α respectively, which kept the sustained activation of IL-6/STAT3 signaling and increased the expression of HIF-1α. Consequently, HIF-1α up-regulated SNAI1 expression, induced EMT, and then accelerated the growth and metastases of the residue HCC cells and attenuated the anti-HCC effect of DOX during TACE.