ArticleBritish journal of cancer2026
Multi-scale transcriptomic integration reveals LINC00152-high tumor cells promote TGCT progression and T cell exhaustion.
Article in British journal of cancer, 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
backgroundTesticular germ cell tumors (TGCTs) are the most common solid malignancies in young men, yet effective biomarkers and therapeutic targets remain limited. The role of lncRNAs in TGCT remains poorly understood at single-cell resolution.
methodsWe integrated single-nucleus RNA-seq, spatial transcriptomics, and bulk RNA-seq on TGCT samples. LINC00152 function was assessed by siRNA knockdown, functional assays, CHIRP-MS, RIP-PCR, and xenograft models. T cell exhaustion was assessed by co-culture experiments and recombinant protein rescue assays.
resultsLINC00152 was identified as a significantly upregulated lncRNA in TGCT, particularly in non-seminomas, and its high expression correlated with advanced tumour stage, lymph node metastasis, and poor prognosis. A LINC00152-high tumour subpopulation showed enhanced proliferation, migration, invasion, and antioxidant capacity. Mechanistically, LINC00152 directly bound to YBX1, inhibiting its proteasomal degradation and thereby activating AKT signaling. Silencing LINC00152 suppressed malignancy in vitro and in vivo. LINC00152-high tumour cells highly expressed HLA molecules and upregulated HAVCR2, promoting T cell exhaustion with reduced IFNG/GZMK expression, rescued by recombinant HAVCR2.
conclusionsLINC00152 serves as a promising prognostic biomarker and therapeutic target in TGCT. It promotes tumour malignancy via YBX1/AKT signaling and drives immune evasion by inducing HAVCR2-mediated T cell exhaustion, providing new insights for combination immunotherapy in TGCT.
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