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Hepatoma-derived growth factor/nucleolin axis as a novel oncogenic pathway in liver carcinogenesis

San-Cher Chen1, Tsung-Hui Hu2, Chao-Cheng Huang3

  • 1Center for Neuroscience, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.

Oncotarget
|May 5, 2015
PubMed

Insights

Hepatoma-derived growth factor (HDGF) binds to nucleolin (NCL) on cancer cells, promoting liver cancer growth. Blocking NCL may offer a new therapeutic strategy for hepatocellular carcinoma (HCC).

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Hepatoma-derived growth factor (HDGF) is implicated in liver fibrosis and carcinogenesis.
  • The specific receptors and signaling pathways activated by HDGF are not fully understood.

Purpose of the Study:

  • To identify the HDGF receptor on hepatoma cells.
  • To elucidate the role of nucleolin (NCL) in HDGF signaling and hepatocellular carcinoma (HCC) pathogenesis.

Main Methods:

  • Affinity chromatography and proteomic techniques to identify HDGF-interacting proteins.
  • Immunohistochemical analysis of HCC tissues.
  • RNA interference for gene knockdown.
  • Assessment of oncogenic behaviors and PI3K/Akt signaling pathways.

Main Results:

  • Nucleolin (NCL) was identified as a membrane protein interacting with HDGF in hepatoma cells.
  • HDGF binding induced NCL accumulation and upregulation, promoting HCC progression and activating PI3K/Akt signaling.
  • NCL overexpression in HCC tissues correlated with advanced tumor grade, vascular invasion, elevated alpha-fetoprotein, and poorer patient survival.
  • NCL acts as an independent prognostic factor for HCC patient survival.

Conclusions:

  • Surface NCL acts as a receptor for HDGF, transmitting oncogenic signals in hepatoma cells.
  • NCL plays a crucial role in liver carcinogenesis by mediating HDGF-induced PI3K/Akt activation.
  • NCL represents a potential novel diagnostic and therapeutic target for HCC.
Keywords:
hepatocellular carcinomahepatoma-derived growth factornucleolintumour progression

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