ArticleBMC cancer2026
Downregulation of THRB drives immune microenvironment suppression and poor outcomes, acting as a dual biomarker for clear cell renal cell carcinoma.
Article in BMC 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
backgroundClear cell renal cell carcinoma (ccRCC) frequently resists targeted and immune therapies, necessitating predictive biomarkers. Thyroid hormone receptor beta (THRB), a nuclear transcription factor at 3p21-25, shows tumor-suppressive roles in other cancers but its immunomodulatory function in ccRCC remains unclear.
methodsUsing TCGA-KIRC data (535 tumors, 72 normals) and validation cohorts (GSE46699/53757), we analyzed THRB expression, clinical correlations, and immune associations via differential expression (limma), survival analysis (Kaplan-Meier/Cox regression), immune infiltration (CIBERSORT/ESTIMATE), functional enrichment (GO/KEGG/GSEA), and drug sensitivity (pRRophetic).
resultsTHRB was significantly downregulated in ccRCCand 11 other cancers (P < 0.05), correlating with advanced stage/grade (P < 0.001) and poorer survival (OS HR = 2.33, DSS HR = 3.43; P < 0.001). Multivariate analysis confirmed its independent prognostic value (HR = 0.69, P = 0.007). Functionally, THRB associated with immune regulation (T-cell activation, PD-1/PD-L1 pathways) and distinct immune infiltration patterns. High-THRB tumors were enriched for resting immune cells and M2 macrophages, while low-THRB tumors showed higher fractions of CD8⁺ T cells and regulatory T cells (Tregs), along with elevated expression of T-cell exhaustion markers (all P < 0.01). This suggests a complex role for THRB in shaping the immune landscape. THRB negatively correlated with TMB (r=-0.26, P < 0.001) and inhibitory checkpoints (LGALS9, CD70), but positively with VTCN1. In silico analysis predicted that low-THRB patients might exhibit reduced sensitivity to sunitinib/pazopanib (higher IC50, P < 0.001).
conclusionTHRB downregulation is associated with poor prognosis, an immunosuppressive microenvironment, and resistance to targeted therapies in ccRCC. These findings suggest its potential as a dual biomarker, implying that THRB loss may contribute to immune dysregulation and therapy resistance. Restoring THRB-mediated pathways may offer novel therapeutic strategies, though its predictive value for immunotherapy requires future clinic validation.
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