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Hypoxia is known to promote malignant progression and to induce chemoresistancein cancer. However, the exact mechanisms driving hypoxia induced malignance remainelusive. We found that with exposure to hypoxic condition, hepatocellular carcinoma(HCC) cells experienced epithelial-mesenchymal transition (EMT), with increasedcell migration and invasion, and exhibited high resistance to chemotherapy. Wedemonstrated that hypoxia-induced EMT and chemoresistance were accompanied byincreased HIF-1α expression and activation of Akt. HIF-1α could be blocked byPI3K inhibitor LY294002, indicating HIF-1α activation was regulated by PI3K/Aktpathway. Furthermore, we showed that inhibition of PI3K/Akt and HIF-1α enhancedthe therapeutic efficacy of hypoxic chemotherapy in the HCC xenograft model. Ourfindings indicate that the activation of PI3K/Akt/HIF-1α pathway plays a criticalrole in mediating hypoxia-induced EMT and drug resistance leading to unfavorabletreatment outcome. Our study provides novel insights into the malignant progressiontriggered by hypoxic microenvironment in HCC cells.

international journal of oncology

Activation of PI3 kinase/Akt/HIF-1α pathway contributes to hypoxia-induced epithelial-mesenchymal transition and chemoresistance in hepatocellular carcinoma