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News
Scientists at Wake Forest have pinpointed a protein called SIRPα that appears to help triple-negative breast cancer (TNBC) spread to the brain and dodge the immune system. In preclinical models, higher SIRPα levels made cancer cells more mobile and suppressed the brain's immune defenses. The findings, published in Neuro-Oncology, open a potential new avenue for treating one of breast cancer's most difficult complications.
Researchers at Wake Forest University School of Medicine have identified a surprising new role for SIRPα — a protein previously known mainly for regulating immune cells — inside triple-negative breast cancer (TNBC) cells themselves. Published in Neuro-Oncology, the preclinical study found that elevated SIRPα levels made TNBC cells more aggressive and more likely to metastasize to the brain, while simultaneously weakening the brain's own immune defenses.
The mechanism works on two fronts. First, SIRPα triggers mitochondrial fission — breaking mitochondria into smaller fragments — which increases cancer cell mobility. Second, it ramps up production of fibronectin, a structural protein that gradually dulls the response of microglia, the brain's resident immune cells, making it harder for them to attack incoming tumor cells. In preclinical models, inhibiting SIRPα slowed tumor growth, reduced brain tumor burden, and partially restored immune function.
Key Takeaways:
Why it matters: Brain metastases from TNBC are notoriously hard to treat. Identifying SIRPα as a driver of both tumor spread and immune evasion gives researchers a compelling new target — one that could potentially be combined with immunotherapy to improve outcomes for patients with advanced TNBC.
