The survival grip-how cell adhesion promotes tumor maintenance within the microenvironment.

Autor: Gardano L; INSERM U978, Bobigny, France.; UFR SMBH Universite Sorbonne Paris Nord, Bobigny, France., Ferreira J; INSERM U978, Bobigny, France.; UFR SMBH Universite Sorbonne Paris Nord, Bobigny, France., Le Roy C; INSERM U978, Bobigny, France.; UFR SMBH Universite Sorbonne Paris Nord, Bobigny, France., Ledoux D; INSERM U978, Bobigny, France.; UFR SMBH Universite Sorbonne Paris Nord, Bobigny, France., Varin-Blank N; INSERM U978, Bobigny, France.; UFR SMBH Universite Sorbonne Paris Nord, Bobigny, France.
Jazyk: angličtina
Zdroj: FEBS letters [FEBS Lett] 2024 Dec 20. Date of Electronic Publication: 2024 Dec 20.
DOI: 10.1002/1873-3468.15074
Abstrakt: Cell adhesion is warranted by proteins that are crucial for the maintenance of tissue integrity and homeostasis. Most of these proteins behave as receptors to link adhesion to the control of cell survival and their expression or regulation are often altered in cancers. B-cell malignancies do not evade this principle as they are sustained in relapsed niches by interacting with the microenvironment that includes cells and their secreted factors. Focusing on chronic lymphocytic leukemia and mantle cell lymphoma, this Review delves with the molecules involved in the dialog between the adhesion platforms and signaling pathways known to regulate both cell adhesion and survival. Current therapeutic strategies disrupt adhesive structures and compromise the microenvironment support to tumor cells, rendering them sensitive to immune recognition. The development of organ-on-chip and 3D culture systems, such as spheroids, have revealed the importance of mechanical cues in regulating signaling pathways to organize cell adhesion and survival. All these elements contribute to the elaboration of the crosstalk of lymphoma cells with the microenvironment and the education processes that allow the establishment of the supportive niche.
(© 2024 Federation of European Biochemical Societies.)
Databáze: MEDLINE
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