ArticleScientific reports2025
Potential role of TNFRSF12A in linking glioblastoma and alzheimer's disease via shared tumour suppressor pathways.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Conserved Pathways, Divergent Outcomes: A Cross-Species Genomic Perspective on the Cancer-Neurodegeneration Paradox.International journal of molecular sciences · 2026Review
- Unraveling the structure-activity relationships of organometallic ferrocene-pyrazole and ferrocene-pyrimidine curcumin analogues in amyloid-β aggregation and glioblastoma treatment.Scientific reports · 2025Article
- Advancing CIK cell immunotherapy: highlights from the second international conference on DC-CIK and CAR-CIK approaches.Cancer immunology, immunotherapy : CII · 2025Article
- Over-Expression of TNFRSF12A Promotes Immune Suppression and Facilitates Angiogenesis in Triple-Negative Breast Cancer.Biology · 2025Article
- Spatial transcriptomics of glioblastoma defines biologically and clinically significant reprogramming patterns across unique spatial microenvironments.bioRxiv : the preprint server for biology · 2025Article
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10 authors.
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Abstract
Tumor suppressor genes (TSGs) are critical regulators of cellular homeostasis and are extensively studied in cancer biology. However, their roles in neurodegenerative diseases, particularly Alzheimer's disease (AD), remain poorly understood. Recent evidence of an inverse association between cancer and AD suggests the existence of shared molecular mechanisms. We conducted an integrative analysis to identify TSGs with potential involvement in both AD and glioblastoma (GBM), using Mendelian randomization, transcriptomic profiling (bulk and single-cell RNA-seq), cell-cell communication inference, and in vitro validation. Among 1,217 TSGs screened, TNFRSF12A was consistently dysregulated in both GBM and AD datasets. Further analysis revealed its association with immune-related pathways and transcriptional programs relevant to both diseases. Knockdown of TNFRSF12A in glioma cells altered the expression of genes associated with amyloid precursor protein (APP) processing and Wnt signaling pathways. This study identifies TNFRSF12A as a cross-disease candidate gene in GBM and AD, based on transcriptomic convergence and partial functional validation. Our findings suggest that TSGs may contribute to shared molecular programs in neurodegeneration and cancer, and warrant further mechanistic investigation.
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