Fenofibrate suppresses growth of the human hepatocellular carcinoma cell via PPARα-independent mechanisms.

摘要: Fenofibrate, a peroxisome proliferator-activated receptor (PPAR) α agonist, is hypolipidemic drug. Although several studies have explored the fenofibrate-induced antiproliferative effect in cultured human cells, it not clear which role PPARα plays this effect. Therefore, we investigated mechanism of fenofibrate Huh7 (human hepatoma cell line). Cell viability was measured by WST-8 assay and proliferation assessed using BrdU incorporation assay. The cycle analyzed flow cytometry. cyclins, tumor suppressor proteins regulators AKT signaling pathway were immunoblotting. Using cytometry, showed that blocks entry into S phase cycle. We certified G1 arrest caused reduction cyclin A E2F1 accumulation cyclin-dependent kinase inhibitor p27. Interestingly, affected antagonist (GW6471) or PPARα-specific siRNA. These results suggest suppresses growth through independent mechanism. Furthermore, treatment cells with leads to suppression phosphorylation. also found for first time increased C-terminal modulator protein (CTMP), inhibits Our data blocking Akt activation, CTMP one key players property cells.