ArticleJournal of translational medicine2026
Targeting C5AR1 disrupts complement-driven G0-phase maintenance and overcomes metabolic drug resistance in glioma.
Article in Journal of translational medicine, 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
backgroundGlioblastoma (GBM) relapse and drug resistance are driven by a subset of quiescent, therapy-tolerant cells that persist in the G0 phase. However, the molecular mechanism coupling immune signaling to tumor cell quiescence and metabolic adaptation remains unclear.
methodsMulti-omics analyses of TCGA, CGGA, and GEO datasets, combined with single-cell transcriptomics and in vitro/in vivo experiments, were used to identify complement-related regulators of G0 maintenance. Genetic manipulation (shRNA/overexpression), pharmacological inhibition (C5AR1 antagonist JPE1375; STAT3 inhibitor Stattic), and rescue experiments with recombinant C3 were performed in glioma cell lines and xenograft models. Cell-cycle, mitochondrial, and redox states were assessed by flow cytometry, immunofluorescence, MitoTracker/MitoSOX staining, and ELISA.
resultsC5AR1 expression was markedly upregulated in GBM and correlated with poor prognosis (HR = 2.7, p = 6.4 × 10
conclusionsC5AR1 links extracellular complement activation to intracellular G0-phase maintenance and metabolic resilience in glioma. Targeting the C3-C5-C5AR1 axis disrupts quiescence-driven drug tolerance and represents a promising therapeutic strategy for overcoming chemoresistance in GBM.
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