RT Journal Article
T1 Tumor vessel co-option probed by single-cell analysis.
A1 Teuwen, Laure-Anne
A1 De Rooij, Laura P M H
A1 Cuypers, Anne
A1 Rohlenova, Katerina
A1 Dumas, Sébastien J
A1 García-Caballero, Melissa
A1 Meta, Elda
A1 Amersfoort, Jacob
A1 Taverna, Federico
A1 Becker, Lisa M
A1 Veiga, Nuphar
A1 Cantelmo, Anna Rita
A1 Geldhof, Vincent
A1 Conchinha, Nadine V
A1 Kalucka, Joanna
A1 Treps, Lucas
A1 Conradi, Lena-Christin
A1 Khan, Shawez
A1 Karakach, Tobias K
A1 Soenen, Stefaan
A1 Vinckier, Stefan
A1 Schoonjans, Luc
A1 Eelen, Guy
A1 Van Laere, Steven
A1 Dewerchin, Mieke
A1 Dirix, Luc
A1 Mazzone, Massimiliano
A1 Luo, Yonglun
A1 Vermeulen, Peter
A1 Carmeliet, Peter
K1 anti-angiogenic therapy
K1 cancer cells
K1 endothelial cells
K1 macrophages
K1 metastasis
K1 pericytes
K1 resistance
K1 single-cell RNA sequencing
K1 tumor angiogenesis
K1 tumor vessel co-option
AB Tumor vessel co-option is poorly understood, yet it is a resistance mechanism against anti-angiogenic therapy (AAT). The heterogeneity of co-opted endothelial cells (ECs) and pericytes, co-opting cancer and myeloid cells in tumors growing via vessel co-option, has not been investigated at the single-cell level. Here, we use a murine AAT-resistant lung tumor model, in which VEGF-targeting induces vessel co-option for continued growth. Single-cell RNA sequencing (scRNA-seq) of 31,964 cells reveals, unexpectedly, a largely similar transcriptome of co-opted tumor ECs (TECs) and pericytes as their healthy counterparts. Notably, we identify cell types that might contribute to vessel co-option, i.e., an invasive cancer-cell subtype, possibly assisted by a matrix-remodeling macrophage population, and another M1-like macrophage subtype, possibly involved in keeping or rendering vascular cells quiescent.
YR 2021
FD 2021
LK https://hdl.handle.net/10668/27805
UL https://hdl.handle.net/10668/27805
LA en
DS RISalud
RD Apr 7, 2025