ArticleClinical and translational medicine2026
ZFP36L1 promotes non-small cell lung cancer progression under hypoxia by modulating CXCL9:SPP1 polarity: A single-cell transcriptomic study.
Article in Clinical and 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
backgroundNon-small cell lung cancer (NSCLC) is the predominant lung cancer subtype with high mortality rate. Drug resistance and immune evasion limit its therapeutic outcomes. Specific mechanism of the oncogenic ZFP36L1 in NSCLC remains unclear.
methodsscRNA-seq data were analysed using bioinformatic approaches. Hypoxia-induced alterations in the macrophage CXCL9:SPP1 ratio were assessed by qRT-PCR, Western blot (WB), immunofluorescence, flow cytometry and ELISA. Dual-luciferase reporter and ChIP assays were used to validate ZFP36L1-mediated transcriptional regulation of SPP1. In a co-cultivation system of macrophages and NSCLC cells, tumour cell malignancy was evaluated through flow cytometry, CCK-8, Transwell, colony formation and scratch assays. Patient-derived organoids co-cultured with macrophages were analysed via H&E, EdU and CellTiter-Glo assays for pathological changes, proliferation and viability, as well as qRT-PCR and WB for the expression of apoptosis-related proteins. Finally, through a macrophage-specific ZFP36L1-knockout mouse model, the function of ZFP36L1 in CXCL9:SPP1 polarity and NSCLC progression was validated in vivo.
resultsHypoxia induced an imbalanced macrophage CXCL9:SPP1 ratio, with more pro-tumour SPP1
conclusionUnder hypoxia, ZFP36L1 transcriptionally regulates SPP1 to reduce the macrophage CXCL9:SPP1 ratio, thereby driving NSCLC malignancy.
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