ArticleCell death discovery2025
TKT drives renal cell carcinoma progression through metabolic reprogramming and synergistic interaction with PKM2.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07450833 (Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine), which is not on this map. Cited by 3 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.
Assessing the Safety, Tolerability and Pharmacokinetics of Benfo-Oxythiamine (B-OT) in Healthy Volunteers - An Open Label, Phase I Study
Who cites it
3 citing papers in PubMed.
- KIF7 promotes the proliferation of clear cell renal cell carcinoma by activating the WNT/β-catenin signaling pathway.Clinical and experimental medicine · 2026Article
- PKM2-Mediated Glycolytic Reprogramming in Thyroid Cancer: Mechanistic Insights and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
- RGS19 drives tumor progression and immunosuppression in clear cell renal cell carcinoma by modulating CAMs and EMT.World journal of surgical oncology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal cell carcinoma (RCC) undergoes profound metabolic reprogramming to fuel its aggressive progression and metastatic dissemination. While transketolase (TKT), a central metabolic enzyme, has been shown to exert dichotomous roles as either oncogenic or tumor-suppressive factors across different malignancies, its functional significance in RCC pathogenesis remains inadequately defined. In this study, we demonstrate that TKT promotes glucose metabolism in RCC by enhancing glycolysis, thereby supporting tumor progression. TKT expression is significantly elevated in RCC tissues and correlates with poor patient prognosis. Mechanistically, we uncovered a novel functional axis between TKT and the glycolytic gatekeeper pyruvate kinase M2 (PKM2), where their coordinated action drives metastatic progression and metabolic adaptation in RCC. Knockdown of PKM2 significantly impaired the TKT-mediated increases in glycolysis, cell proliferation, and invasive potential. Taken together, our findings highlight TKT as a pivotal regulator of metabolic reprogramming in RCC and suggest its potential as a therapeutic target for the treatment of this malignancy.
Identifiers
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Registered trials
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