Fig. 1

Function of Del-1 in cancer and inflammation. The framed section represents the tumor microenvironment and the unframed section represents inflammatory conditions. (1) Del-1 is correlated with the invasion and metastasis of some cancers through FAK, TGF-β, ERK, or other unknown signaling pathways; (2) Del-1 in the bone marrow niche binds to HSCs αvβ3 integrin on one end and interacts with the extracellular matrix at the other end, thus promoting HSC proliferation and differentiation into the myeloid lineage; (3) In the in-vessel lumen, endothelial cell-derived Del-1 blocks the binding of αLβ2 (LFA-1) integrin to ICAM-1 on vascular endothelial cells, thereby blocking the adhesion and migration of neutrophils. Some studies have found that Del-1 can also block αMβ2 (Mac-1) integrin, which mediates neutrophil crawling in the official cavity; (4) In the course of the resolution of inflammation, neutrophils transform into apoptotic cells after exerting an anti-inflammatory effect. Del-1 connects PS on apoptotic cells at one end, which is an “eat-me” signal, and αvβ3 integrin on macrophages at the other end as a bridge for cell-to-cell communication to promote the uptake of apoptotic cells by macrophages. Del-1 developmental endothelial locus-1, EVs extracellular vesicles, HSCs hematopoietic stem cells, MyP myeloid progenitors, ECM extracellular matrix, ICAM intercellular adhesion molecule, PS phosphatidylserine