Adelaide University Researchers Discover Dual-Action Protein Mechanism Fueling Aggressive Glioblastoma Tumor Invasion

A new study identifies how the CD47 protein drives glioblastoma spread by protecting ROBO2, opening a new molecular pathway for brain cancer treatment.

By: AXL Media

Published: Mar 24, 2026, 4:56 AM EDT

Source: Information for this report was sourced from Adelaide University

Beyond Immune Evasion: A New Role for CD47

Glioblastoma remains one of the most lethal challenges in oncology, with standard treatments like surgery and chemotherapy often failing to prevent recurrence within 18 months. While the protein CD47 has long been recognized as a "don't eat me" signal that helps tumors bypass the immune system, researchers at Adelaide University’s Centre for Cancer Biology have uncovered a much more aggressive internal function. Published in PNAS, the study reveals that CD47 acts as a direct driver of tumor proliferation and migration. According to senior author Dr. Nirmal Robinson, the protein is particularly abundant at the invasive edges of tumors, where it facilitates the spread of cancer into healthy brain tissue, directly correlating with poorer patient survival outcomes.

The Discovery of the CD47-ITCH-ROBO2 Pathway

The research team identified a previously unknown molecular chain of command that dictates how glioblastoma cells behave. At the center of this mechanism is a partner protein called ROBO2, which is essential for the cancer's ability to move and invade. Under normal cellular conditions, a protein known as ITCH would tag ROBO2 for destruction, keeping tumor growth in check. However, the study found that CD47 effectively shields ROBO2 by sequestering ITCH. This protective "shield" allows ROBO2 to accumulate to dangerous levels, fueling the rapid progression of the disease. Dr. Ruhi Polara, who co-led the research, noted that when CD47 is removed, the cellular machinery is once again able to degrade ROBO2, causing cancer cells to lose their invasive edge.

Evidence from Immune-Independent Models

To confirm that this growth was not solely dependent on the immune system's failure, the team utilized laboratory experiments and animal models where immune cells were absent. Even in these environments, blocking CD47 dramatically reduced the speed at which tumors grew and spread. In some instances, the survival time in these models nearly doubled once the CD47-ROBO2 connection was disrupted. This evidence shifts the scientific understanding of CD47 from being a simple immune checkpoint to a central regulator of internal tumor biology. The findings suggest that the protein's presence is a fundamental requirement for the structural and migratory integrity of glioblastoma cells.