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Peer-reviewedCC BY 4.0Pediatric Surgery International

Heparan sulphate expression in high-risk neuroblastoma

  • Valeria Solari1,2
  • Lucia Borriello3
  • Jeremy E. Turnbull4
  • Edwin A. Yates2
4 affiliations
  1. 1Independent researcher, Vienna, Austria
  2. 2Department of Biochemistry, Cell and Systems Biology, Institute of Integrative Biology, University of Liverpool, Crown Street, Liverpool, L69 7ZB UK
  3. 3Department of Cancer and Cellular Biology, Lewis Katz School of Medicine, Cancer Signaling and Microenvironment Program, Fox Chase Cancer Center, Philadelphia, USA
  4. 4Centre for Glycocalyx Research, University of Copenhagen, Copenhagen, Denmark
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Abstract

Purpose: Heparan sulphate proteoglycans (HSPGs) regulate tumour cell interactions with the microenvironment. Sulfatase-2 (SULF2), an extracellular endosulfatase that modifies heparan sulphate (HS) 6-O-sulphation, has been implicated in neuroblastoma (NBL), particularly in high risk MYCN-amplified (MYCN-A) tumours. We investigated HS distribution in NBL and the effects of SULF2 knockdown on tumour cell behaviour.

Methods: HS expression was analysed in NBL cell lines using the anti HS antibody 10E4 and the phage display antibody HS3A8V. Cell migration was assessed following siRNA mediated SULF2 knockdown. HS expression in 65 primary human NBL specimens was quantified by colour deconvolution and compared by MYCN status and histological risk groups.

Results: HS epitopes were abundantly expressed on NBL cell surfaces, particularly in MYCN-A SK-N-BE(2) cells and localised along intercellular extensions. SULF2 knockdown significantly reduced cell migration, particularly in MYCN-A cells (p < 0.01), altered HS staining and reduced intercellular extensions. In primary MYCN-A tumours showed significantly greater 10E4 immunoreactivity than MYCN-non-amplified (NA) tumours with favourable or unfavourable histology (both p < 0.0001), with no difference between the latter groups.

Conclusion: MYCN-A NBL demonstrates a distinct HS phenotype. SULF2-mediated HS remodelling may contribute to tumour cell migration and HS-rich intercellular extensions, identifying SULF2 as a potential therapeutic target in high-risk NBL.

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Cite

BibTeXRIS
BibTeX
@article{solari2026heparan,
  title = {{Heparan sulphate expression in high-risk neuroblastoma}},
  author = {Valeria Solari and Lucia Borriello and Jeremy E. Turnbull and Edwin A. Yates},
  journal = {Pediatric Surgery International},
  year = {2026},
  month = nov,
  doi = {10.1007/s00383-026-06700-3},
  url = {https://doi.org/10.1007/s00383-026-06700-3},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Heparan sulphate expression in high-risk neuroblastoma
AU  - Valeria Solari
AU  - Lucia Borriello
AU  - Jeremy E. Turnbull
AU  - Edwin A. Yates
PY  - 2026
DA  - 2026/11/03
JO  - Pediatric Surgery International
DO  - 10.1007/s00383-026-06700-3
UR  - https://doi.org/10.1007/s00383-026-06700-3
AB  - Purpose: Heparan sulphate proteoglycans (HSPGs) regulate tumour cell interactions with the microenvironment. Sulfatase-2 (SULF2), an extracellular endosulfatase that modifies heparan sulphate (HS) 6-O-sulphation, has been implicated in neuroblastoma (NBL), particularly in high risk MYCN-amplified (MYCN-A) tumours. We investigated HS distribution in NBL and the effects of SULF2 knockdown on tumour cell behaviour.  Methods: HS expression was analysed in NBL cell lines using the anti HS antibody 10E4 and the phage display antibody HS3A8V. Cell migration was assessed following siRNA mediated SULF2 knockdown. HS expression in 65 primary human NBL specimens was quantified by colour deconvolution and compared by MYCN status and histological risk groups.  Results: HS epitopes were abundantly expressed on NBL cell surfaces, particularly in MYCN-A SK-N-BE(2) cells and localised along intercellular extensions. SULF2 knockdown significantly reduced cell migration, particularly in MYCN-A cells (p < 0.01), altered HS staining and reduced intercellular extensions. In primary MYCN-A tumours showed significantly greater 10E4 immunoreactivity than MYCN-non-amplified (NA) tumours with favourable or unfavourable histology (both p < 0.0001), with no difference between the latter groups.  Conclusion: MYCN-A NBL demonstrates a distinct HS phenotype. SULF2-mediated HS remodelling may contribute to tumour cell migration and HS-rich intercellular extensions, identifying SULF2 as a potential therapeutic target in high-risk NBL.
SN  - 0179-0358
SN  - 1437-9813
ER  -