ArticleFrontiers in oncology2026
UBA1 enhances phagocytosis by suppressing CD47 expression in small cell lung cancer.
Article in Frontiers in oncology, 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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Abstract
Introduction: Small cell lung cancer (SCLC) exhibits a limited overall response rate to immunotherapy, largely due to its highly immunosuppressive microenvironment. CD47, an innate immune checkpoint frequently overexpressed on SCLC cells, contributes to immune evasion by inhibiting macrophage-mediated phagocytosis. Here, we uncover a previously unrecognized immunoregulatory function of ubiquitin-like modifier activating enzyme 1 (UBA1) in SCLC. Methods: We analyzed UBA1 expression in 16 SCLC patients undergoing immunotherapy (immunohistochemistry). Functional studies used UBA1-knockdown and overexpression SCLC cell lines (H446, H82) to assess phagocytosis, macrophage polarization, and CD47 regulation. Mechanistic insights were obtained via Hippo pathway activation assays (enhancing MST1/YAP phosphorylation). Results: High UBA1 expression correlated with improved immunotherapy response and prolonged progression-free survival. UBA1 activates the Hippo signaling pathway, enhancing MST1 and YAP phosphorylation and thereby repressing CD47 transcription. UBA1 overexpression attenuates surface CD47 levels in SCLC cells, potentiates macrophage phagocytic activity, and promotes a pro-inflammatory macrophage polarization, whereas UBA1 knockdown exerts opposing effects. Conclusion: UBA1 enhances phagocytosis by suppressing CD47 through the Hippo-YAP pathway, improving immunotherapy efficacy in SCLC. Collectively, these findings reveal that the UBA1-CD47 axis represents a potentially pathway in SCLC and UBA1 may serve as a candidate biomarker and a potential mechanistic node for therapeutic intervention.
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