Prevention of hepatocellular carcinoma by correction of metabolic abnormalities: Role of statins and metformin

Core Tip

Core tip: Hepatocellular carcinoma is the result of a complex process which impairs several pathways, such as RAS/RAF/mitogen-activated protein kinase kinase/extracellular-signal-regulated kinase, phosphatidylinositol-4,5-bisphosphate 3-kinase/AKT/mammalian target of rapamycin and Wnt/β-catenin signaling. Patients showing metabolic syndrome seem to have higher incidence and mortality rates from hepatocellular carcinoma than healthy subjects, especially those with type 2 diabetes mellitus and obesity. Thus, metformin and statins, both to treat features of metabolic syndrome, have been proposed to decrease the risk of hepatocellular carcinoma. Metformin (by decreasing hyperglycemia state through 5′-adenosine monophosphate-activated protein kinase pathway activation) and statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) show anti-tumoral properties modifying several steps of the crucial signaling cascades.