Evidence map›Paper›PMID 38590281›Full record

ArticleCancer science2024

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

Yue Guo, Yutaka Kasai, Yuto Tanaka, Yuki Ohashi-Kumagai, Takeharu Sakamoto, Takeshi Ito, Yoshinori Murakami

Abstract read
In one paragraph

Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. Article
  2. The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Yue GuoDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yutaka KasaiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yuto TanakaDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Yuki Ohashi-KumagaiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Takeharu SakamotoDepartment of Cancer Biology, Institute of Biomedical Science, Kansai Medical University, Hirakata, Japan.ORCID https://orcid.org/0000-0002-1225-1902
Takeshi ItoDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0003-2404-3825
Yoshinori MurakamiDivision of Molecular Pathology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan.ORCID https://orcid.org/0000-0002-2826-4396

Funding

Japan Agency for Medical Research and Development 20ae0101073Japan Agency for Medical Research and Development JP22ama221307Japan Society for the Promotion of Science 20H03525Japan Society for the Promotion of Science 20H05028Japan Society for the Promotion of Science 20K21539Japan Society for the Promotion of Science 21K07091
6 · The paper itself

Abstract

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.

Indexed as

Endothelium, VascularLung NeoplasmsMelanoma, ExperimentalAnimalsCell AdhesionCell Adhesion MoleculesCell Line, TumorGene Knockdown TechniquesHumansImmunoglobulinsMembrane ProteinsMiceMice, Inbred C57BLCell Adhesion MoleculesIGSF3 protein, humanImmunoglobulinsMembrane Proteinsadhesionimmunoglobulin superfamilymelanomametastasisvascular endothelium

Identifiers

PMID38590281
PMCPMC11145127

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.