ArticleCell death and differentiation2026
LGALS1-CD276 Paracrine axis between tumor and endothelial cells promotes tumor angiogenesis and progression in bladder cancer.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Authors and funding
16 authors.
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Abstract
Bladder cancer, particularly muscle-invasive disease, has a high metastatic potential and limited treatment options, highlighting the need for new therapeutic targets. CD276 (B7-H3), a type I transmembrane protein of the B7 family, is traditionally considered an immunomodulatory ligand with an unidentified receptor. Here, we investigated the role of CD276 in bladder cancer and sought to identify its binding partner. Using a high-throughput human proteome microarray, we identified the secreted lectin galectin-1 (LGALS1) as a high-affinity binding partner of CD276, suggesting that CD276 may function as a receptor. Mechanistically, we uncovered a novel LGALS1-CD276 axis in endothelial cells, where CD276 serves as a functional receptor for tumor cell-derived LGALS1, with their interaction mediated by N-linked glycosylation at the N433 site within the D4 domain of CD276. This interaction activates the MAP4-dependent PI3K/AKT signaling pathway, thereby promoting angiogenesis and bladder cancer progression. Disruption of the LGALS1-CD276 interaction or inhibition of the downstream MAP4/PI3K/AKT pathway markedly suppressed endothelial proliferation, migration, and tube formation. In subcutaneous and orthotopic bladder cancer mouse models, anti-CD276 monoclonal antibody treatment significantly inhibited tumor angiogenesis, delayed tumor growth, and extended survival. Consistently, Cd276
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