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hSulf-1 gene exhibits anticancer efficacy through negatively regulating VEGFR-2 signaling in human cancers

Weidan Ji1, Jiahe Yang, Duanming Wang

  • 1Department of Molecular Oncology, Eastern Hepatobiliary Surgical Hospital & Institute, The Second Military Medical University, Shanghai, China.

Plos One
|August 20, 2011
PubMed
Abstract

Insights

Human sulfatase 1 (hSulf-1) inhibits cancer cell proliferation and tumor growth by reducing VEGFR-2 phosphorylation and suppressing angiogenesis. This suggests hSulf-1 is a potential therapeutic target for cancer treatment.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Human sulfatase 1 (hSulf-1) is an enzyme that modifies cell surface heparan sulfate proteoglycans.
  • hSulf-1 influences growth factor signaling, but its precise role in cancer is not fully understood.

Purpose of the Study:

  • To investigate the role of hSulf-1 in regulating vascular endothelial growth factor receptor (VEGFR) signaling.
  • To explore the potential of hSulf-1 as a therapeutic agent in cancer.

Main Methods:

  • Generated vectors for hSulf-1 re-expression and knockdown using small hairpin RNA (shRNA).
  • Utilized ovarian and hepatocellular cancer cell lines for in vitro studies.
  • Assessed tumor growth and microvessel density in human cancer xenografts in nude mice.

Main Results:

  • hSulf-1 re-expression downregulated VEGFR-2 phosphorylation and inhibited cancer cell proliferation.
  • Knockdown of hSulf-1 enhanced VEGFR-2 phosphorylation, while VEGFR-2 knockdown partially inhibited proliferation.
  • In vivo studies showed significant tumor growth inhibition (46-49%) and reduced tumor microvessel density with hSulf-1 expression.

Conclusions:

  • hSulf-1 re-expression demonstrates antitumor efficacy by attenuating VEGFR-2 phosphorylation and suppressing angiogenesis.
  • hSulf-1-mediated anti-proliferation and anti-angiogenesis present a viable strategy for cancer therapy.

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