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Related Experiment Video

Updated: May 11, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

Published on: June 16, 2018

ADAM12-cleaved ephrin-A1 contributes to lung metastasis.

K Ieguchi¹, T Tomita¹, T Omori¹

¹Department of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.

|May 21, 2013

Summary

This summary is machine-generated.

The EphA1/ephrin-A1 system promotes cell adhesion and lung metastasis by maintaining cell contacts and increasing vascular permeability. Soluble ephrin-A1, enhanced by ADAM12, drives this process, which can be blocked by neutralizing antibodies.

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Last Updated: May 11, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues

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Published on: June 16, 2018

Lung Tumor Cell Recruitment Assay

Lung Tumor Cell Recruitment Assay

Published on: February 26, 2019

Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

Eph receptor tyrosine kinases and ephrin ligands are crucial in development and neovascularization.
Ephrin-A1 overexpression correlates with tumor progression and poor prognosis, but underlying mechanisms remain unclear.

Purpose of the Study:

To elucidate the role of the Eph/ephrin system in cell adhesion and its contribution to tumor metastasis.
To identify molecular mechanisms linking EphA1/ephrin-A1 signaling to tumor progression and vascular permeability.

Main Methods:

Investigated EphA1/ephrin-A1 complex behavior (endocytosis, cell adhesion) in pulmonary endothelial cells.
Utilized yeast two-hybrid screening to identify EphA1-binding partners.
Assessed the impact of ADAM12 and transforming growth factor-β1 on ephrin-A1 cleavage.
Evaluated the effect of soluble ephrin-A1 and neutralizing antibodies on lung metastasis and vascular permeability in vivo.

Main Results:

Clustered EphA1/ephrin-A1 complexes resist endocytosis, maintaining cell-cell adhesion independently of Eph tyrosine kinase activity and E-cadherin.
EphA1 and ephrin-A1 co-localize in pulmonary endothelial cells, regulating vascular permeability and lung metastasis.
ADAM12 was identified as an EphA1-binding partner that enhances ephrin-A1 cleavage in response to TGF-β1.
Soluble ephrin-A1 promotes lung hyperpermeability and metastasis in an endocrine manner, which is significantly inhibited by its neutralizing antibody.

Conclusions:

The Eph/ephrin system mediates cell adhesion through non-degradative plasma membrane complexes.
ADAM12-mediated cleavage of ephrin-A1 contributes to lung metastasis by increasing vascular permeability.
Targeting soluble ephrin-A1 presents a potential therapeutic strategy to inhibit tumor metastasis.