Emerging roles of FGF signaling in hepatocellular carcinoma.

作者: Wenyi Wei , Nana Zheng , Zhiwei Wang

DOI: 10.21037/6391

关键词: Hepatocellular carcinomaBioinformaticsFibroblast growth factor receptorPI3K/AKT/mTOR pathwayEpidermal growth factorFibroblast growth factorMedicineLiver cancerSorafenibPlatelet-derived growth factor receptorCancer research

摘要: Liver cancer is the fifth most common malignance in world. It has been known that 90% of liver cancers are hepatocellular carcinoma (HCC). estimated more than 740,000 new cases HCC were diagnosed and approximately 700,000 deaths occurred worldwide. In USA, 35,660 people will be with 24,550 patients die from year 2015. China, 400,000 developed 370,000 due to this deadly disease. Although surgical resection transplantation have improved, 5-year survival rate no significant decrease part fact late stage at diagnosis. Additionally, many exhibit low sensitivity standard radiotherapy chemotherapy. For example, sorafenib drug for treatment advanced cases; however, median overall these still less 1 partly resistance. Therefore, it pivotal discover therapeutic drugs patients. Emerging evidence suggested hepatitis C virus (HCV) B (HBV) infection important risk factors incidence HCC. addition, obesity, diabetes nonalcoholic steatohepatitis found contribute incidence. Without a doubt, presence cirrhosis overriding factor recent years, several lines defined some genes cellular signaling pathways play key role development progression HCC, including Notch, PI3K (phosphatidylinositol 3-Kinase)/Akt, extracellularregulated kinase (ERK), mammalian target rapamycin (mTOR), mitogen-activated protein (MAPK), Hedeghog, Wnt pathways. Moreover, growth such as epidermal (EGF), hepatocyte (HGF), insulin-like (IGF), transforming (TGF), platelet-derived (PDGF) fibroblast (FGF) also emerged critical players tumorigenesis carcinogenesis. Among pathways, FGF recently gained high attention progression. article, we briefly describe advances physiological function molecular mechanism We present current chemical inhibitors FGF/FGFR natural agents inactivate pathway. Lastly, discuss whether could prognostic markers and/ or potential targets

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