ArticleCell proliferation2026
PIK-III-Mediated Elevation of Thiamine Re-Sensitises Renal Cell Carcinoma to Cuproptosis via Activating PDHA1.
Article in Cell proliferation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Amplifying bacterial cuproptosis by NIR driven biomimetic metal organic framework for nanocatalytic enhanced bacterial pneumonia immunotherapy.Bioactive materials · 2026Article
- Copper Metabolism-Related Cell Death in Kidney Diseases: Molecular Mechanisms, Disease-Specific Evidence, and Translational Implications.International journal of molecular sciences · 2026Review
- TMEM72 Inhibits the proliferation by promoting cellular senescence through the activation of the P38/MAPK signaling pathway in renal cell carcinoma.Translational oncology · 2026Article
- CuET promotes cuproptosis and ferroptosis of lung cancer cells by interacting directly with polyunsaturated phospholipids.iScience · 2026Article
- PIK-III-Mediated Elevation of Thiamine Re-Sensitises Renal Cell Carcinoma to Cuproptosis via Activating PDHA1.Cell proliferation · 2026Article
- Cuproptosis-triggering nanomedicine boosts antitumor immunotherapy.Theranostics · 2026Review
- Succinylation in cancer immunotherapy: mechanisms, biomarkers, and therapeutic implications.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Cuproptosis, a copper-dependent cell death mechanism driven by tricarboxylic acid (TCA) cycle collapse, shows limited efficacy in hypoxic or glycolytic renal cell carcinoma (RCC). Here, through systematic screening of 688 glycolysis inhibitors combined with elesclomol (ES), we identified PIK-III as a potent cuproptosis sensitiser. Multi-omics analysis revealed that PIK-III restores sensitivity by rewiring thiamine metabolism. Mechanistically, PIK-III induces macropinocytosis, enabling thiamine uptake to replenish thiamine pyrophosphate (TPP), which activates pyruvate dehydrogenase E1-alpha 1 (PDHA1) and redirects pyruvate into the TCA cycle. Concurrently, ES-induced DLAT oligomerisation disrupts TCA flux, creating a metabolic crisis. In vivo, PIK-III synergises with ES to suppress tumour growth in xenograft and patient-derived models without systemic toxicity. Our work uncovers a metabolic vulnerability in cuproptosis-resistant RCC and positions PIK-III as a therapeutic candidate to overcome resistance via dual targeting of thiamine transport and mitochondrial dysfunction.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.