IGSF3 is a homophilic cell adhesion molecule that drives lung metastasis of melanoma by promoting adhesion to vascular endothelium.

adhesion immunoglobulin superfamily melanoma metastasis vascular endothelium

Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
09 Apr 2024
Historique:
revised: 14 03 2024
received: 09 11 2023
accepted: 20 03 2024
medline: 9 4 2024
pubmed: 9 4 2024
entrez: 9 4 2024
Statut: aheadofprint

Résumé

The immunoglobulin superfamily (IgSF) is one of the largest families of cell-surface molecules involved in various cell-cell interactions, including cancer-stromal interactions. In this study, we undertook a comprehensive RT-PCR-based screening for IgSF molecules that promote experimental lung metastasis in mice. By comparing the expression of 325 genes encoding cell-surface IgSF molecules between mouse melanoma B16 cells and its highly metastatic subline, B16F10 cells, we found that expression of the immunoglobulin superfamily member 3 gene (Igsf3) was significantly enhanced in B16F10 cells than in B16 cells. Knockdown of Igsf3 in B16F10 cells significantly reduced lung metastasis following intravenous injection into C57BL/6 mice. IGSF3 promoted adhesion of B16F10 cells to vascular endothelial cells and functioned as a homophilic cell adhesion molecule between B16F10 cells and vascular endothelial cells. Notably, the knockdown of IGSF3 in either B16F10 cells or vascular endothelial cells suppressed the transendothelial migration of B16F10 cells. Moreover, IGSF3 knockdown suppressed the extravasation of B16F10 cells into the lungs after intravenous injection. These results suggest that IGSF3 promotes the metastatic potential of B16F10 cells in the lungs by facilitating their adhesion to vascular endothelial cells.

Identifiants

pubmed: 38590281
doi: 10.1111/cas.16166
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Agency for Medical Research and Development
ID : 20ae0101073
Organisme : Japan Agency for Medical Research and Development
ID : JP22ama221307
Organisme : Japan Society for the Promotion of Science
ID : 20H03525
Organisme : Japan Society for the Promotion of Science
ID : 20H05028
Organisme : Japan Society for the Promotion of Science
ID : 20K21539
Organisme : Japan Society for the Promotion of Science
ID : 21K07091

Informations de copyright

© 2024 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Yue Guo (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yutaka Kasai (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yuto Tanaka (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yuki Ohashi-Kumagai (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Takeharu Sakamoto (T)

Department of Cancer Biology, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.

Takeshi Ito (T)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Yoshinori Murakami (Y)

Division of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.

Classifications MeSH