TY - JOUR
T1 - Dynamic Interactions between Tumor Cells and Brain Microvascular Endothelial Cells in Glioblastoma
AU - Testa, Erika
AU - Palazzo, Claudia
AU - Mastrantonio, Roberta
AU - Viscomi, Maria Teresa
PY - 2022
Y1 - 2022
N2 - GBM is the most aggressive brain tumor among adults. It is characterized by extensive vascularization, and its further growth and recurrence depend on the formation of new blood vessels. In GBM, tumor angiogenesis is a multi-step process involving the proliferation, migration and differentiation of BMECs under the stimulation of specific signals derived from the cancer cells through a wide variety of communication routes. In this review, we discuss the dynamic interaction between BMECs and tumor cells by providing evidence of how tumor cells hijack the BMECs for the formation of new vessels. Tumor cell–BMECs interplay involves multiple routes of communication, including soluble factors, such as chemokines and cytokines, direct cell–cell contact and extracellular vesicles that participate in and fuel this cooperation. We also describe how this interaction is able to modify the BMECs structure, metabolism and physiology in a way that favors tumor growth and invasiveness. Finally, we briefly reviewed the recent advances and the potential future implications of some high-throughput 3D models to better understanding the complexity of BMECs–tumor cell interaction.
AB - GBM is the most aggressive brain tumor among adults. It is characterized by extensive vascularization, and its further growth and recurrence depend on the formation of new blood vessels. In GBM, tumor angiogenesis is a multi-step process involving the proliferation, migration and differentiation of BMECs under the stimulation of specific signals derived from the cancer cells through a wide variety of communication routes. In this review, we discuss the dynamic interaction between BMECs and tumor cells by providing evidence of how tumor cells hijack the BMECs for the formation of new vessels. Tumor cell–BMECs interplay involves multiple routes of communication, including soluble factors, such as chemokines and cytokines, direct cell–cell contact and extracellular vesicles that participate in and fuel this cooperation. We also describe how this interaction is able to modify the BMECs structure, metabolism and physiology in a way that favors tumor growth and invasiveness. Finally, we briefly reviewed the recent advances and the potential future implications of some high-throughput 3D models to better understanding the complexity of BMECs–tumor cell interaction.
KW - angiogenesis
KW - cancer
KW - endothelial cells
KW - extracellular vesicles
KW - miRNA
KW - neovascularization
KW - tumor vessels normalization
KW - angiogenesis
KW - cancer
KW - endothelial cells
KW - extracellular vesicles
KW - miRNA
KW - neovascularization
KW - tumor vessels normalization
UR - http://hdl.handle.net/10807/231401
U2 - 10.3390/cancers14133128
DO - 10.3390/cancers14133128
M3 - Article
SN - 2072-6694
VL - 14
SP - 3128
EP - 3145
JO - Cancers
JF - Cancers
ER -