@article{10902/32845,
year = {2024},
url = {https://hdl.handle.net/10902/32845},
abstract = {Neoplastic progression involves complex interactions between cancer cells and the surrounding stromal milieu, fostering microenvironments that crucially drive tumor progression and dissemination. Of these stromal constituents, cancer-associated fibroblasts (CAFs) emerge as predominant inhabitants within the tumor microenvironment (TME), actively shaping multiple facets of tumorigenesis, including cancer cell proliferation, invasiveness, and immune evasion. Notably, CAFs also orchestrate the production of pro-angiogenic factors, fueling neovascularization to sustain the metabolic demands of proliferating cancer cells. Moreover, CAFs may also directly or indirectly affect endothelial cell behavior and vascular architecture, which may impact in tumor progression and responses to anti-cancer interventions. Conversely, tumor endothelial cells (TECs) exhibit a corrupted state that has been shown to affect cancer cell growth and inflammation. Both CAFs and TECs are emerging as pivotal regulators of the TME, engaging in multifaceted biological processes that significantly impact cancer progression, dissemination, and therapeutic responses. Yet, the intricate interplay between these stromal components and the orchestrated functions of each cell type remains incompletely elucidated. In this review, we summarize the current understanding of the dynamic interrelationships between CAFs and TECs, discussing the challenges and prospects for leveraging their interactions towards therapeutic advancements in cancer.},
organization = {Funding: Spanish Government MCIN/AEI/10.13039/501100011033 (grants RYC-2016‐20352, RTI2018‐096778‐A‐I00, PID2021‐ 128107OB‐I00); Asociación Española Contra el Cáncer-AECC (grants LABAE19044CALV, PRYCO211372RODR); BBVA Leonardo Awards (grant IN [19]_BBM_BAS_0076), Cancer Research UK (grant C57744/A22057); and the European Research Council-ERC Consolidator Grant antiCAFing (grant ref 101045756). Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature.
Acknowledgements: The authors would like to thank all members of the FC laboratory for help, support and discussions associated with this manuscript. We also thank Emad Moeendarbary and his lab members (UCL, London, UK) for key contributions in current CAF-TEC projects within FC laboratory. We are grateful for financial support by Spanish Government MICIU/AEI/10.13039/501100011033 (grants RYC‐2016‐20352, RTI2018‐096778‐A‐I00, PID2021‐128107OB‐ I00); Asociación Española Contra el Cáncer-AECC (grants LABAE-19044CALV, PRYCO211372RODR); BBVA Leonardo Awards (grant IN[19]_BBM_BAS_0076), Cancer Research UK (grant C57744/ A22057); and the European Research Council-ERC Consolidator Grant antiCAFing (grant 101045756). DC has been a recipient of a Boehringer Ingelheim Fonds PhD Travel Grant. Finally, we would like to dedicate this work to the memory of David Alburquerque Gutiérrez. He was a great friend whose humanity will continue to inspire us.},
publisher = {Springer Nature},
publisher = {Cellular Oncology, 2024},
title = {CAFs vs. TECs: when blood feuds fuel cancer progression, dissemination and therapeutic resistance},
author = {Coursier, Diane Léonie and Calvo González, Fernando},
}