ArticleFrontiers in immunology2026
UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma.
Article in Frontiers in immunology, 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: LINC00887 plays critical roles in tumor biology, from oncogenesis to metastasis and drug resistance, while the specific mechanism in ccRCC remains unclear. We analyzed the expression profiles of LINC00887 and UPF1 and assessed their correlation with glycolytic activity and M2 macrophage infiltration. Methods: Here, we performed scRNA-seq to identify distinct UPF1 expression profiles and found significant pathways. A suite of assay kits was utilized to evaluate glycolytic metabolism. Glycolytic gene expression at the mRNA and protein levels was quantified via qRT-PCR and immunoblot. Macrophage polarization and CD8 Results: We found that highly expressed LINC00887 induced M2 macrophage polarization by activating aerobic glycolysis and promoting lactate buildup. Mechanistically, suppression of UPF1 expression promoted malignant progression of ccRCC. Additionally, UPF1 was found to be negatively correlated with aerobic glycolysis, repressing glycolytic activity and M2 macrophage polarization while bolstering the tumor-killing potential of CD8 Conclusion: In summary, LINC00887, through the inhibition of UPF1, escalates glycolytic activity in ccRCC and induces M2 macrophage polarization, impairing the effectiveness of CD8
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