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Related Experiment Video

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Tumor vessel co-option probed by single-cell analysis.

Laure-Anne Teuwen1, Laura P M H De Rooij2, Anne Cuypers2

  • 1Laboratory of Angiogenesis and Vascular Metabolism, Center for Cancer Biology (CCB), VIB, Department of Oncology, Leuven Cancer Institute, KU Leuven, Leuven 3000, Belgium; Translational Cancer Research Unit, GZA Hospitals Sint-Augustinus, Antwerp 2610, Belgium; Center for Oncological Research, University of Antwerp, Antwerp 2000, Belgium.

Cell Reports
|June 16, 2021
PubMed
Summary

Tumor vessel co-option, a resistance to anti-angiogenic therapy (AAT), involves complex cell interactions. This study reveals unexpected similarities in co-opted cells, identifying potential roles for cancer and myeloid cells in tumor growth.

Keywords:
anti-angiogenic therapycancer cellsendothelial cellsmacrophagesmetastasispericytesresistancesingle-cell RNA sequencingtumor angiogenesistumor vessel co-option

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Tumor vessel co-option is a poorly understood mechanism of resistance to anti-angiogenic therapy (AAT).
  • The cellular heterogeneity within co-opted vessels and surrounding cells in AAT-resistant tumors has not been explored at a single-cell level.

Purpose of the Study:

  • To investigate the cellular and molecular landscape of AAT-resistant lung tumors employing vessel co-option.
  • To identify distinct cell populations contributing to the vessel co-option process using single-cell RNA sequencing.

Main Methods:

  • Utilized a murine model of AAT-resistant lung cancer where VEGF-targeting therapy promotes vessel co-option.
  • Performed single-cell RNA sequencing (scRNA-seq) on 31,964 cells from the tumor microenvironment.

Main Results:

  • Found that co-opted tumor endothelial cells (TECs) and pericytes exhibit transcriptomes largely similar to their healthy counterparts.
  • Identified an invasive cancer cell subtype potentially driving co-option.
  • Discovered a matrix-remodeling macrophage population possibly aiding co-option and an M1-like macrophage subtype potentially maintaining vascular cell quiescence.

Conclusions:

  • Tumor vessel co-option in this model is not driven by significant transcriptomic changes in endothelial cells or pericytes.
  • Specific cancer and myeloid cell subtypes play crucial roles in facilitating and maintaining vessel co-option during AAT resistance.