Abstract
Hepatitis B virus (HBV) infection plays a crucial role and is a major cause of hepatocellular carcinoma (HCC) in China. microRNAs (miRNAs) have emerged as key players in hepatic steatosis and carcinogenesis. We found that down-regulation of miR-384 expression was a common event in HCC, especially HBV-related HCC. However, the possible function of miR-384 in HBV-related HCC remains unclear. The oncogene pleiotrophin (PTN) was a target of miR-384. HBx inhibited miR-384, increasing PTN expression. The PTN receptor N-syndecan was highly expressed in HCC. PTN induced by HBx acted as a growth factor via N-syndecan on hepatocytes and further promoted cell proliferation, metastasis and lipogenesis. PTN up-regulated sterol regulatory element-binding protein 1c (SREBP-1c) through the N-syndecan/PI3K/Akt/mTORC1 pathway and the expression of lipogenic genes, including fatty acid synthesis (FAS). PTN-mediated de novo lipid synthesis played an important role in HCC proliferation and metastasis. PI3K/AKT and an mTORC1 inhibitor diminished PTN-induced proliferation, metastasis and lipogenesis. Taken together, these data strongly suggest that the dysregulation of miR-384 could play a crucial role in HBV related to HCC, and the target gene of miR-384, PTN, represents a new potential therapeutic target for the prevention of hepatic steatosis and further progression to HCC after chronic HBV infection.
Keywords:
hepatitis B virus; hepatocellular carcinoma; lipogenesis; metastasis; miR-384; pleiotrophin.
© 2017 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
MeSH terms
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Adult
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Carcinoma, Hepatocellular / etiology
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Carcinoma, Hepatocellular / genetics*
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Carcinoma, Hepatocellular / metabolism
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Carcinoma, Hepatocellular / pathology
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Carrier Proteins / genetics*
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Carrier Proteins / metabolism
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Cell Proliferation
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Chromones / pharmacology
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Cytokines / genetics*
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Cytokines / metabolism
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Female
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Gene Expression Regulation, Neoplastic*
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Hep G2 Cells
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Hepatitis B / complications
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Hepatitis B / genetics*
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Hepatitis B / metabolism
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Hepatitis B / pathology
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Hepatitis B virus / pathogenicity
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Hepatitis B virus / physiology
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Hepatocytes / drug effects
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Hepatocytes / metabolism
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Hepatocytes / pathology
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Host-Pathogen Interactions*
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Humans
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Lipogenesis / drug effects
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Lipogenesis / genetics
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Liver Neoplasms / etiology
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Liver Neoplasms / genetics*
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Liver Neoplasms / metabolism
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Liver Neoplasms / pathology
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Lymphatic Metastasis
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Male
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Mechanistic Target of Rapamycin Complex 1 / antagonists & inhibitors
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Mechanistic Target of Rapamycin Complex 1 / genetics
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Mechanistic Target of Rapamycin Complex 1 / metabolism
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MicroRNAs / genetics*
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MicroRNAs / metabolism
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Middle Aged
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Morpholines / pharmacology
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Phosphatidylinositol 3-Kinases / genetics
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Phosphatidylinositol 3-Kinases / metabolism
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Phosphoinositide-3 Kinase Inhibitors
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Proto-Oncogene Proteins c-akt / antagonists & inhibitors
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Signal Transduction
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Sirolimus / pharmacology
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Sterol Regulatory Element Binding Protein 1 / genetics
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Sterol Regulatory Element Binding Protein 1 / metabolism
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Syndecan-3 / genetics
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Syndecan-3 / metabolism
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Trans-Activators / genetics
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Trans-Activators / metabolism
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Trans-Activators / pharmacology
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Viral Regulatory and Accessory Proteins
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fas Receptor / genetics
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fas Receptor / metabolism
Substances
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Carrier Proteins
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Chromones
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Cytokines
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FAS protein, human
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MIRN384 microRNA, human
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MicroRNAs
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Morpholines
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Phosphoinositide-3 Kinase Inhibitors
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Sterol Regulatory Element Binding Protein 1
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Syndecan-3
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Trans-Activators
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Viral Regulatory and Accessory Proteins
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fas Receptor
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hepatitis B virus X protein
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pleiotrophin
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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Mechanistic Target of Rapamycin Complex 1
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Proto-Oncogene Proteins c-akt
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Sirolimus