Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide. More than 90% of HCCs develop as a result of chronic liver disease, and chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is the main cause in most areas. However, several studies in Western countries showed that 30–40% of patients with HCC do not have chronic HBV or HCV infections . Although this cluster includes alcoholic liver injury and some genetic liver diseases, such as hemochromatosis, other cases are more likely to be associated with obesity and metabolic syndrome and are considered to be based on nonalcoholic steatohepatitis (NASH). Additionally, obesity increased the risk of HCC development in patients with viral hepatitis . Because its prevalence has been increasing worldwide, obesity’s potential association with hepatocarcinogenesis has attracted considerable attention in recent years. Although the mechanism by which obesity and metabolic syndrome promote hepatocarcinogenesis is not fully understood, it seems likely to be mediated, in part, by a state of chronic inflammation [3,4]. Importantly, recent evidence revealed that endoplasmic reticulum (ER) stress is a key link between metabolism and inflammation in obesity-driven hepatocarcinogenesis.
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