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ampk/pka/gsk-3beta-mediated c-flipl degradation glucose-ampk-tet2-5hmc axis participate weicheng wu & jianxin gu ampk/pka/gsk-3β initiate pre-metastatic sites hetero-trimeric kinase modulated fast-growing hepatocellular carcinomas abundant mir-25-3p sds-polyacrylamide gel electrophoresis potent anti-angiogenic activities tcr/cd3/zeta complex enzyme-linked immunosorbent assays 400-mesh carbon-coated grid transmembrane ca2+-binding protein amp-activated protein kinase cgmp-pkg signaling pathway hepatocellular carcinoma/peritumor samples vegf165/vegfr2-dependent signaling transcriptome-based molecular classifications metastatic oral cancer article download pdf n-cadherin tcga-lihc exo-3b-kd treated bel-7402 clec3b-mediated vegf expression cd63-positive secretory vesicles crisper-cas9-px260-clec3b hepatocellular carcinoma progression molecular biology human hepatocellular carcinoma genome-wide survey privacy choices/manage cookies type culture collection pre-existing vessels endothelial cell medium named exo-3b-kd ampk/mtor signaling pathway exosome-mediated transfer real-time pcr independent prognostic factor nonparenchymal liver cells nat rev cancer creative commons license clec3b rt p1 epithelial–mesenchymal transition related subjects glycoconjugate research ministry stimulate kinase activity disease-free survival time full access poor prognostic factor

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• Vascular and haematopoietic stem cells: novel targets for anti-angiogenesis therapy?

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         headline:Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals
         description:C-Type Lectin Domain Family 3 Member B (CLEC3B), is down-regulated in serum and tumor tissues in different cancers including hepatocellular carcinoma (HCC). However, the functions of CLEC3B in HCC remains elucidated. The aim of this study is to analyze the roles of CLEC3B in HCC. The expression of genes was evaluated by immunohistochemistry, western blot, real-time PCR, enzyme-linked immunosorbent assays, and analysis on TCGA-LIHC database and gene expression omnibus. Transmission electron microscopy and immunofluorescence were applied to detect CLEC3B in exosomes. The function of exosomal CLEC3B in tumor progression were performed in vivo and in vitro. We determined that down-regulated CLEC3B in HCC indicated a poor prognosis. Exosomes derived from HCC with down-regulated CLEC3B promoted migration, invasion, epithelial–mesenchymal transition of both tumor cells and endothelial cells (ECs). Moreover, the downregulation CLEC3B in exosomes suppressed VEGF secretion in both HCC cells and ECs, and eventually inhibited angiogenesis. Mechanistically, CLEC3B-mediated VEGF expression in tumor cells and ECs depends on the activation of AMPK signal pathway. This study demonstrates that CLEC3B acts as a novel independent prognostic factor, and CLEC3B in exosomes might be a potential therapeutic target for hepatocellular carcinoma.
         datePublished:2019-09-02T00:00:00Z
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      headline:Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals
      description:C-Type Lectin Domain Family 3 Member B (CLEC3B), is down-regulated in serum and tumor tissues in different cancers including hepatocellular carcinoma (HCC). However, the functions of CLEC3B in HCC remains elucidated. The aim of this study is to analyze the roles of CLEC3B in HCC. The expression of genes was evaluated by immunohistochemistry, western blot, real-time PCR, enzyme-linked immunosorbent assays, and analysis on TCGA-LIHC database and gene expression omnibus. Transmission electron microscopy and immunofluorescence were applied to detect CLEC3B in exosomes. The function of exosomal CLEC3B in tumor progression were performed in vivo and in vitro. We determined that down-regulated CLEC3B in HCC indicated a poor prognosis. Exosomes derived from HCC with down-regulated CLEC3B promoted migration, invasion, epithelial–mesenchymal transition of both tumor cells and endothelial cells (ECs). Moreover, the downregulation CLEC3B in exosomes suppressed VEGF secretion in both HCC cells and ECs, and eventually inhibited angiogenesis. Mechanistically, CLEC3B-mediated VEGF expression in tumor cells and ECs depends on the activation of AMPK signal pathway. This study demonstrates that CLEC3B acts as a novel independent prognostic factor, and CLEC3B in exosomes might be a potential therapeutic target for hepatocellular carcinoma.
      datePublished:2019-09-02T00:00:00Z
      dateModified:2019-09-02T00:00:00Z
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         Exosomes
         Hepatocellular carcinoma
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         AMPK
         Cell Biology
         Protein-Ligand Interactions
         Receptors
         Cytokines and Growth Factors
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      name:Key Laboratory of Glycoconjugate Research Ministry of Health; Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China
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      name:Key Laboratory of Glycoconjugate Research Ministry of Health; Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China

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