M-CSFR expression in the embryonal component of hepatoblastoma and cell-to-cell interaction between macrophages and hepatoblastoma

Lianbo Li, Tomoaki Irie, Daiki Yoshii, Yoshihiro Komohara, Yukio Fujiwara, Shigeyuki Esumi, Masashi Kadohisa, Masaki Honda, Shinya Suzu, Toshiharu Matsuura, Kenichi Kohashi, Yoshinao Oda, Taizo Hibi

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Tumor-associated macrophages (TAMs) have protumor functions in various cancers. However, their significance in hepatoblastoma, the most common liver tumor in children, remains unclear. The aim of this study was to explore the potential roles of TAMs in hepatoblastoma. Immunohistochemical analysis revealed that the density of CD204-positive TAMs was significantly higher in the embryonal component than in other histological subtypes of hepatoblastoma. An in vitro co-culture study with Huh6 cells and human monocyte-derived macrophages (HMDMs) showed that macrophage-colony-stimulating factor receptor (M-CSFR) was strongly up-regulated in the Huh6 cells that were directly co-cultured with HMDMs. The expressions of M-CSFR ligands (interleukin-34 and M-CSF) were also increased by co-culture with HMDMs. The proliferation of HepG2 cells (another hepatoblastoma cell line expressing M-CSFR) was inhibited by an M-CSFR inhibitor. M-CSFR was found to be highly expressed in the embryonal component and in recurrent lesions. The number of CD204-positive macrophages was also higher in the M-CSFR-positive areas than in the M-CSFR-negative areas. Thus, M-CSFR expression appeared to be induced by cell–cell contact with macrophages in hepatoblastoma cells, and M-CSFR inhibitor is potentially effective against M-CSFR-positive hepatoblastoma, especially recurrent cases.

Original languageEnglish
Pages (from-to)236-247
Number of pages12
JournalMedical Molecular Morphology
Volume55
Issue number3
DOIs
Publication statusPublished - Sept 2022

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine
  • Molecular Biology

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