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Activation of AKT-AP1-FOXM1 signaling pathway confers sorafenib resistance to hepatocellular carcinoma cells

Xiaojing Yan  Lingxi Chen  Liangbo Sun  Tao Li  Fengtian He  Jiqin Lian  
【摘要】:Sorafenib is the first-line drug for advanced hepatocellular carcinoma(HCC),but the clinical response to sorafenib is seriously limited by drug resistance.In this study,we investigated the molecular mechanisms of sorafenib resistance in HCC cells.Our data indicate that FoxM1 was significantly over-expressed in sorafenib-resistant cells,both at mRNA and protein levels.Knockdown of FoxM1 made drug-tolerant cells sensitive to sorafenib.Furthermore,we found that FOXM1 was upregulated at transcriptional level.And the overexpression of c-jun was associated with the up-regulation of FOXM1.The binding site of AP1 in the promoter of FOXM1 located at-608--618.Knockdown of c-jun significantly decreased the level of FOXM1 accompanied with enhanced cell sensitivity to sorafenib.Moreover,the activation of AKT contributed to the upregulation of c-jun and FOXM1.Inhibitor of AKT BEZ-235 dramatically suppressed the up-regulation of c-jun and FOXM1,and increased the sensitivity of drug-tolerant cells to sorafenib in vitro and in vivo.Our data imply that the activation of AKTAP1-FOXM1 signaling axis is an important determinant of sorafenib tolerance.

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