Remodeling the sarcoma microenvironment by simultaneous targeting of urokinase-type plasminogen activator receptors and epidermal growth factor receptors to promote antitumor activity.

ABSTRACT: We evaluated the antitumor effects of remodeling the MC17 mouse sarcoma microenvironment (SME) by targeting urokinase-type plasminogen activator receptor (uPAR)- and epidermal growth factor receptor (EGFR)-expressing cells. Specifically, we used eBAT (a bispecific ligand-targeted toxin directed to EGFR and uPAR), and its mouse counterpart, meBAT, to ablate uPAR- and/or EGFR-expressing cells. We chose the MC17 model because the cells are resistant to eBAT, allowing us to exclusively evaluate the role of uPAR- and EGFR-expressing cells in the SME. Our results show that uPAR expression, both by the tumor cells and by the SME, was dispensable for tumor formation. However, uPAR-deficient tumors grew considerably slower than uPAR-expressing tumors. To specifically address mechanisms responsible

SUBMITTER: Schulte AJ 

PROVIDER: S-EPMC12597637 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature