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A Co-opted Developmental Gene Regulatory Program in Endothelial Progenitors Promotes Tumor Angiogenic Phenotypes.

Andrew J Lee¹, Sunwoo Min¹, Su Chan Park²

¹Korea Advanced Institute of Science & Technology Daejeon Korea (South), Republic of.

Cancer Research

|June 8, 2026

Summary

Tumor-associated endothelial cells (TECs) reactivate a developmental gene program from endothelial cell (EC) progenitors. This reprogramming, mediated by integrin αv, drives tumor angiogenesis and offers a therapeutic target.

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Published on: May 11, 2021

Area of Science:

Endothelial cell biology
Cancer research
Developmental biology

Background:

Endothelial cells (ECs) transition to tumor-associated endothelial cells (TECs), promoting tumor progression.
Understanding the mechanisms of TECs is crucial for identifying therapeutic targets.

Purpose of the Study:

To reveal the gene regulatory programs driving TEC angiogenic phenotypes.
To identify key mediators of endothelial plasticity in the tumor microenvironment (TME).

Main Methods:

Analysis of single-cell transcriptomic and epigenomic atlases from solid tumors.
Projection of TEC gene programs onto human embryonic stem cell (hESC)-derived EC differentiation maps.
Stimulation of primary ECs with TME ligands and integrin αv inhibition.

Main Results:

TECs reactivate an EC progenitor gene program for extracellular matrix (ECM) remodeling.
Integrin αv acts as a mediator of endothelial plasticity in the TME.
Inhibition of integrin αv suppressed endothelial migration, invasion, and tumor vascularization.

Conclusions:

Tumor endothelial plasticity is driven by co-opted developmental cis-regulatory programs.
This highlights a mechanism for TEC adaptation in tumors.
Targeting this reprogramming offers a therapeutic strategy against tumor angiogenesis.