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The role of HGF/MET in liver cancer

机译：The role of HGF/MET in liver cancer

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Liver cancer is the sixth most prevalent form of cancer worldwide and the third leading cause of cancer-related death [1]. Chronic hepatitis due to excessive alcohol intake, autoimmune hepatitis, hepatitis (B and C) infections, primary biliary cirrhosis, non-alcoholic fatty hepatitis, environmental carcinogens and hereditary metabolic disorders are contributing factors for liver cancer [2]. Although the precise mechanism of transformation from healthy liver cells to cancerous liver cells is not well known, carcinogenesis of the liver is a multistep procedure, involving the accumulation of heterogeneous molecular changes, from initial liver cell damage to metastatic invasion [3]. Molecular changes associated with the development of hepatocellular carcinoma (HCC) involve mutations of tumor suppressor genes (p53 and p16) and oncogenes together with epigenetic changes, proliferation, chromosomal changes, invasion, angiogenesis and metastasis, and abnormal activation of signal cascades necessary for survival. The pathogenesis of early and late liver cancer can be regulated by various mechanisms. For example, advanced HCC is more likely to have p16 gene silencing, irregular AKT signaling and p53 mutations [1]. Liver cancer is relatively resistant to cytotoxic chemotherapy, which may be due to multidrug resistance genes, protein products like P-glycoprotein and heat shock 70, and overexpression of p53 mutations. Currently, systemic treatment options in the setting of local progression or metastasis are limited to sorafenib, an oral multikinase inhibitor of tyrosine kinase signaling that targets PDGF, VEGF and RAF kinase [4].

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