GEO series

CD47 activates ROBO2 signaling to regulate glioblastoma cell plasticity and metabolism

GSE282771 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/03/09 Platform GPL18573

Summary

CD47 inhibits phagocytosis by myeloid cells, contributing to immune evasion by cancer cells. Although CD47-blocking antibodies have shown promise in treating various malignancies, their efficacy in glioblastoma (GBM) remains limited, and the role of CD47 beyond immune escape is poorly understood. Here, we show that CD47 is highly expressed at the invasive edge of GBM tumours, with elevated expression correlating with poorer patient survival. We demonstrate that CD47 loss reduces proliferation, migration, and invasion, independently of immune activity leading to decreased GBM tumour burden and prolonged survival in vivo. Mechanistically, our study reveals that CD47 regulates ROBO2 signaling and enhances mitochondrial respiration. Furthermore, we demonstrate that combined loss of CD47 or ROBO2 with inhibition of mitochondrial function significantly increases GBM cell death. These findings highlight CD47 as a key regulator of GBM cell and metabolic plasticity, offering a novel therapeutic strategy by targeting CD47 or ROBO2 in combination with mitochondrial inhibitors.

Published in

CD47 stabilizes ROBO2 to regulate glioblastoma progression by preventing ITCH-mediated ubiquitination

Polara R, Gliddon BL, Ganesan R et al. · Proceedings of the National Academy of Sciences of the United States of America 2026 · PMID 41871254 · doi:10.1073/pnas.2602460123

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Also filed as BioProject PRJNA1190393 and SRA study SRP547400. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41871254) ↗

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