Solitary fibrous tumor/hemangiopericytoma metastasizes extracranially, associated with altered expression of wnt5a and mmp9

Jong Hwan Hong, Myung Giun Noh, Md Rashedunnabi Akanda, Yeong Jin Kim, Se Hoon Kim, Tae Young Jung, Shin Jung, Jae Hyuk Lee, Joon Haeng Rhee, Kyung Keun Kim, Sung Sun Kim, Kyung Hwa Lee, Kyung Sub Moon

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4 Citations (Scopus)


Solitary fibrous tumor/hemangiopericytoma (SFT/HPC) is a mesenchymal tumor originat-ing from various soft tissues and meninges, which carries the NAB2-STAT6 fusion gene. Meningeal/intracranial SFT/HPCs (icSFT/HPC) have a poor clinical outcome with metastatic behav-ior compared to soft tissue/extracranial SFT/HPCs (exSFT/HPC), but the underlying genetic factors are unclear. Differentially expressed genes (DEGs) were analyzed by NanoString nCounter assay using RNA extracted from formalin-fixed paraffin-embedded (FFPE) tissue samples. Additionally, immunohistochemistry (IHC) was performed on 32 cases of exSFT/HPC, 18 cases of icSFT/HPC, and additional recurrent or metastatic cases to verify the findings. Pathway analysis revealed that the WNT signaling pathway was enriched in exSFT/HPC. Analysis of DEGs showed that expression of WNT5A was lower and that of MMP9 was higher in icSFT/HPC than in exSFT/HPC (p = 0.008 and p = 0.035, respectively). IHC showed that WNT5A and CD34 expression was high in exSFT/HPC (p < 0.001, both), while that of MMP9 was high in icSFT/HPC (p = 0.001). Expression of CLDN5 in tumoral vessels was locally decreased in icSFT/HPC (p < 0.001). The results suggested that decreased WNT5A expression, together with increased MMP9 expression, in icSFT/HPC, may affect vascular tightness and prompt tumor cells to metastasize extracranially.

Original languageEnglish
Article number1142
Pages (from-to)1-15
Number of pages15
Issue number5
Publication statusPublished - 2021 Mar 1

Bibliographical note

Funding Information:
This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Minist (2020M3A9G3080281, 2019R1A2B5B01070598, and 2018R1A5A2024181 for K.-H.L., 2020R1C1C1007832 for K.-S.M.) and by Chonnam National University Hospital Biomedical Institute (HCRI19030 for K.-S.M. and K.-H.L.). There was no role of the funding bodies in the design of the study, in the collection, analysis, and interpretation of data or in writing the manuscript.

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research


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