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Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide;however, the prognosis of HCC patients remains poor. This poor prognosis is mainlyattributed to the high rate of intrahepatic and distant metastasis. HCC oftenoccurs in a hypoxic environment and hypoxia can activate metastatic programs,ultimately leading to tumor recurrence or metastasis. Thus, the discovery andsubsequent development of novel agents to block HCC invasion and migration arethe primary objectives of hepatic cancer research. The Notch1 signaling pathwaymight be involved in hypoxia-induced carcinoma metastasis. However, the mechanismsby which Notch1 mediates cell metastasis, particularly in hepatocellular carcinoma,are not yet entirely clear. The results of the present study show that hypoxiaincreases the invasion and migration capacities of different HCC cells. Activationof the Notch1 signaling pathway contributes to hypoxia-induced invasion and migrationin HCC cells. The activated Notch1 signaling pathway can regulate Snail/E-cadherinthrough cyclooxygenase-2 (COX-2) under hypoxic conditions. The above results suggestthat the Notch1/COX-2/Snail/E-cadherin pathway is possibly associated with hypoxia-inducedinvasion and migration in HCC cells. Thus, targeting Notch1 may be useful fordevising novel preventive and therapeutic strategies for HCC.

The Notch1/cyclooxygenase-2/Snail/E-cadherin pathway is associated with hypoxia-induced hepatocellular carcinoma cell invasion and migration