In the present study, the efficacy and specificity of a <sup>125</sup>I-labeled CD93-specific monoclonal antibody (<sup>125</sup>I-anti-CD93 mAb) in detecting NSCLC xenografts were analyzed, and the association between CD93 expression and <sup>125</sup>I-anti-CD93 mAb uptake by tumors was evaluated.
These findings demonstrate a key role of CD93 in vascular maturation and organization of the extracellular matrix in tumors, identifying it as a potential target for therapy.
The C-type lectin domain containing group 14 family members CLEC14A and CD93 are proteins expressed by endothelium and are implicated in tumour angiogenesis.
CD93 expression is functionally required for engraftment of primary human AML LSCs and leukemogenesis, and it regulates LSC self-renewal predominantly by silencing CDKN2B, a major tumor suppressor in AML.
This effect was associated with increased vascular permeability and decreased vascular perfusion of tumors, indicating reduced vessel functionality in the absence of CD93.