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Downregulation of exosomal CLEC3B in hepatocellular carcinoma promotes metastasis and angiogenesis via AMPK and VEGF signals

  • Dai, Wenjuan1
  • Wang, Yilin2
  • Yang, Tianxiao3
  • Wang, Jing1
  • Wu, Weicheng1, 4
  • Gu, Jianxin1
  • 1 School of Basic Medical Sciences, Fudan University, Key Laboratory of Glycoconjugate Research Ministry of Health; Department of Biochemistry and Molecular Biology, Shanghai, China , Shanghai (China)
  • 2 Department of Hepatic Surgery, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China , Shanghai (China)
  • 3 Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Shanghai, China , Shanghai (China)
  • 4 School of Public Health; School of Life Sciences and Human Phenome Institute, Fudan University, The Key Laboratory of Public Health and Safety of Education Ministry, Shanghai, China , Shanghai (China)
Published Article
Cell Communication and Signaling
BioMed Central
Publication Date
Sep 02, 2019
DOI: 10.1186/s12964-019-0423-6
Springer Nature


BackgroundC-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.MethodsThe 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.ResultsWe 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.ConclusionThis study demonstrates that CLEC3B acts as a novel independent prognostic factor, and CLEC3B in exosomes might be a potential therapeutic target for hepatocellular carcinoma.Graphical abstract

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